A Critical Analysis regarding the Innovation Management Practices Adopted by Apple Inc. and Haier Group Free Essay Example, 3500 words

The company has shown a constant openness to new ideas, as they believe that new ideas are not only limited to new product development but are equally significant for the improvement of business processes. The firm believes in this principle has produced highly satisfactory results for the company and by the end of the year 2010. The number of patents and innovation are highest for this company among the Chinese manufacturers (Yuanyuan 2011). A series of initiatives have been taken by the company to promote innovation and creativity at the workplace. All these initiatives of the company revolve around quality and customer satisfaction. An example shows how the company has emphasized upon providing high quality to consumers when it decided to set a quality benchmark even above the Japanese Industrial Standard (JIS). As per the guidelines of JIS, the return-repair ratio for refrigerator should be less than 0.6%, as against this stringent benchmark of JIS, the company decided to set th e same ratio at the level of 0.4%. As a result of this decision the company in the year 1988, Haier was awarded China s National Quality Gold Medal. We will write a custom essay sample on A Critical Analysis regarding the Innovation Management Practices Adopted by Apple Inc. and Haier Group or any topic specifically for you Only $17.96 $11.86/page The management philosophy of OEC was introduced in the year 1986 and became famous with the name of All around Optimized Management Approach (TU and YUAN 2010). The OEC plan was driven by the purpose of effective management of everyday business processes and enabled Haier in evaluating the appropriateness of the plan in terms of produced outcomes.

Future Fuel Is A Small Oil Company Essay - 1379 Words

Future Fuel Future Fuel is a small oil company characterized by individuals who are supporters of sustainability and have legitimate concern for the environment and are also aware of the growing green movement .As a result we have plans of increasing the research and development budget for seeking new renewable and viable alternative sources of energy as well as equipping the headquarters and 8 other sites in the west with renewable energy systems .Questions like what we are aiming to achieve, our position on corporate social responsibility, what the company owe to shareholders ,what return on investment is required, and finally how we shall balance the needs of shareholders and the need to innovate will be examined below; Our mission Sustainability is a major driving force in most businesses today, and the rise of sustainability in the market has brought major economic and financial impact on businesses today. Sustainability as defined by the United Nations is the process of meeting present needs without compromising the ability of future generations to meet their needs. (McKee 2012, page 561). Companies which are considered environmentally unfriendly face a lot of threats when it comes to finance. Therefore oil and gas companies that produce environmental unfriendly bi products face critical supervision from both policy makers and consumers. Given that the stock of Future Fuel has been less than stellar fromShow MoreRelatedThe Problem For Electric Alternatives1323 Words   |  6 Pagescompany is referring to as a trip planner. This piece of technology allows the vehicle to communicate with charging station in the nearby area in an effort to make sure the driver never runs out of battery. The trip planner will alert the driver when and where the vehicle should be charged so that it does not die before reaching a charging station (Davies, 2015). 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Pathogenesis of measles virus infection Free Essays

string(48) " tissue where further viral replication occurs\." Introduction Measles is a highly contagious disease caused by an enveloped RNA virus of the genus Morbillivirus in the family of Paramyxoviridae (Griffin et al, 1994). It is a major cause of child morbidity and mortality, particularly in developing countries, despite the introduction of attenuated measles virus vaccines which have greatly reduced the incidences since the 1960s (WHO, 2009). The window period of infection for infants lies between the disappearing maternal antibody protection and vaccine administration (Manchester and Rall, 2001). We will write a custom essay sample on Pathogenesis of measles virus infection or any similar topic only for you Order Now In 2008, 164,000 measles deaths were reported and majority was children under five years old (WHO, 2009). Affected individuals combat measles by generating cell mediated immunity to clear the virus and humoral immunity to provide long-term protection (Manchester and Rall, 2001). However, measles virus (MV) induces immunosuppression during infection and for weeks after recovery, rendering infected individuals susceptible to secondary infections (Griffin et al, 1994). The evidence of immunosuppression caused was first recognized in 1908 when von Pirquet reported that children lost positive skin test for tuberculin antigen during MV infection (von Pirquet, 1908). Research has been carried in vitro and in vivo in order to define the pathogenesis pathways of MV. Immune responses to MV have been described on transgenic mice and cynomolgus monkeys models (Sato et al, 2007) suggesting that multiple potential mechanisms are linked to the virus-induced immunosuppression (Schneider-Schaulies et al, 2002). Infection Measles is transmitted via airborne exposure from coughing and sneezing or close contact with nasal and throat secretions. MV remains active in the air for up to two hours. It enters the body through the respiratory system and spread systemically by infecting lymphoid cells. Infection and spread is a complex process. The structure and proteins of MV are important determinants of virus tropism and pathogenesis (Yanagi et al, 2006). Measles virus consists of a non-segmented single negative-strand RNA genome (16,000 ribonucleotides) with a diameter of 150 to 300 nm. The outer envelope comprises with the inner matrix protein to form a lipid bilayer surrounding the viral genome. It encodes six structural proteins and two nonstructural proteins which are important for attachment of the virus to the host, replication and spreading of the virus in the body (Horikami et al, 1995). Table 1 briefly describes the functions and locations of structural components and Figure 1 illustrates the structure of a measles virus. Table 1: Locations and functions of Measles virus structural proteins Structural proteins Locations Functions 1. Haemagglutinin(H) Both H and F proteins are surface transmembrane glycoproteins. They project from the lipid bilayer and traverse the internal matrix. Responsible for the initiation of infection. H protein: receptor binding and cell fusion F protein: cell fusion and viral entry. 2. Fusion proteins (F) 3. Nucleoprotein (N)Surround the RNA strandForm a ribonucleocapsid. 4. Phosphoprotein (P) Both P and L proteins are associated with the ribonucleocapsidThe ribonucleoprotein complex acts as RNA polymerase and is responsible for RNA replication and transcription. 5. Large polymerase protein (L) 6. Matrix protein (M)Attaches to the inner surface of the envelopeAssembly of the viral particles. Virus budding. Adapted from (Yanagi et al, 2006) The nonstructural protein C and V are encoded on the P gene by RNA editing and alternative translation. Patterson et al (2000) showed that C and V proteins functioned as virulence factors in CNS measles infection using YAC-CD46 transgenic mice. In addition, C protein is capable to inhibit viral transcription and enhancing MV particles assembly. These proteins have shown to be involved in inhibition of interferon production (Naniche et al, 2000). The infection process involves four steps: 1. Attachment When measles virus enters the respiratory tract, the initial infection begins with viral attachment to host cellular receptors by the haemagglutinin (H) protein. The most studied receptors are CD46 and signaling lymphocytic activation molecule (SLAM/ CD150) (Ferreira et al, 2010). CD46 is a complement regulatory molecule and is present on all nucleated human cells whereas SLAM is only expressed on thymocytes, mature dendritic cells and T and B lymphocytes (Hsu et al, 2001). Other cell surface proteins such as moesin and substance P receptor were also proposed in MV binding (Kehren et al, 2001). The primary target for early stage infection has not been clearly defined. It was originally thought that respiratory epithelial cells were firstly infected (Griffin, 2001) but following the discovery of SLAM, some studies suggested that SLAM-positive immune cells should be the initial targets (Yanagi et al, 2002). Leonard et al. (2008) suggested the presence of a basolateral epithelial recept or (EpR) is necessary for entry of MV into respiratory epithelium and infection of the epithelial cells is required for shedding and transmission. Figure 1: a) Structure of a measles virus b) Measles virus genome c) Membrane fusion and replication of measles virus in a cell Take from the wed-site http://www.nature.com/nrmicro/journal/v4/n12/box/nrmicro1550_BX1.html (Moss Griffin, 2006) 2. Fusion The interaction of both H and F proteins with human receptors is important for the virus to gain access into the host cell. Fusion (F) protein mediates the fusion of viral envelop with cell membrane. Figure 1 (c) demonstrated the fusion process. When the tetramer H protein binds to its receptor, it generates a conformational change within the F protein which is composed of two subunits F1 and F2 linked by a disulphide bond. The activated F protein inserts the hydrophobic fusion peptide into the target cell membrane and provides entry of the viral genome into the host cell interior (Weidmann et al, 1999). 3. RNA replication and Assembly of viral particles The polymerase allows replication and transcription of the genome within the cell. The negative sense RNA is copied into a complementary positive strand which, in turn, acts as a template for the negative strand. Viral components are translated in the cell and are assembled at the cell surface (Yanagi et al, 2006). 4. Release of virus MV leaves the host cell in a budding form (Yanagi et al, 2006). Spread The viremic spread from the respiratory tract is carried out by infected immune cells including monocytes, dendritic cells, B and T cells which travel through the local lymphatics and are transported to the secondary lymphoid tissue where further viral replication occurs. You read "Pathogenesis of measles virus infection" in category "Essay examples" A secondary viremia occurs when infected cells enter the circulation and viral replication continues in the endothelia and epithelia of other organs including skin, gastrointestinal tract, liver, kidney and central nervous system (Ferreira et al, 2010). A systemic spread is favored by the immunosuppression following infection. Multiple mechanisms are involved in the development of immunosuppression and a brief description below focuses on some of the important pathways. 1. Changes in lymphocyte number and function Lymphopenia of B and T cells during viremic and post-clinical recovery stages is demonstrated by many studies. Bieback et al. (2002) showed that MV can bind to Toll-like receptor (TLR) 2 on monocytes, inducing SLAM expression and interleukin-6 (IL-6) production. In addition, binding of SLAM can induce Fas (CD95)-mediated apoptosis of uninfected CD4+ and CD8+ T lymphocytes. The extracellular composition of CD46 is characterized by four short consensus repeat (SCR) and a STP domain. SCRs 2, 3 and 4 are binding regions for C3b and C4b, thereby preventing them from causing autologous complement lysis. The attachment of MV to SCRs 1 and 2 alters the normal signaling pathway resulting in down-regulation of CD46, eventually leading to increased C3b-mediated complement lysis (Manchester and Rall, 2001). MV also inhibits lymphoproliferation by causing cell cycle arrest in the G0/G1 phase in dividing lymphocytes (Niewiesk et al, 1999) and interferes with NF-kB signaling pathways and anti-apoptotic B cell lymphoma 3 (Bcl-3) proteins (Bolt Berg, 2002). Furthermore, Nucleoprotein of MV binds to the Fc-gamma receptor on antigen presenting cells and impairs their ability to stimulate T cell proliferation (Hehren et al, 2001). Figure 2 summarized the main pathways leading to immunosuppression. Figure 2: Mechanisms of immunosuppression following measles virus infection Adapted from (Moss et al, 2004) 2. Shift in cytokine profile Early evasion of the innate immune responses is the interference of interferon-alpha/beta signaling pathways (Naniche et al, 2000) due to inhibition of STAT1 and STAT2 phosphorylation by proteins V and C. However, IFN-gamma production is not affected in the acute phase of measles (Takeuchi et al, 2003). Cross-linking of CD46 by MV and direct binding of MV to CD46 on monocytes and dendritic cells inhibit the production of IL-12 (Karp et al, 1996) and hence suppress macrophage activation, T cell proliferation and delayed-type hypersensitivity (Atabani et al, 2001). The loss of IL-12 also decreases type 1 cytokines TNF-alpha and IL-2, leading to transition to type 2 cytokines IL-4, IL-5 and IL-10 by CD4+ T cells (Moss et al, 2002). Th1 to Th2 shift leads to a change of cell-mediated immunity to a dominant humoral immunity which is not sufficient to combat new infections (Kemper et al, 2003). 3. Impaired antigen presentation Dendritic cells are critical for the antigen presentation to naive T lymphocyte. MV infected dendritic cells fail to undergo differentiation to become mature effector cells and some of them are susceptible to Fas-mediated apoptosis (Servet-Delprat et al, 2000). Marttila et al (2001) reported that antigen processing of other viruses such as rubella virus and coxsackie B4 virus is compromised in MV-infected human mononuclear cells, suggesting impaired antigen presentation to T cells. Symptoms The clinical presentation is induced by the immune responses. The initial encounter of the virus activates the innate immunity with high levels of IFN-? and IL-8 but it is not efficient to clear the virus, leading to rapid multiplication of virus (Sato et al, 2008). Figure 3 illustrates the timeline of viremia and appearance of symptoms. Figure 3: Pathogenesis of measles virus and immune responses of host. Obtained from http://pathmicro.med.sc.edu/mhunt/mump-meas.htm (Hunt, 2008) The early symptoms of measles, listed below, usually appear after an incubation period of 10 to 12 days and last for 2 to 4 days due to inflammatory reactions affecting the respiratory tract and conjunctiva (Griffin, 1995). Fever Malaise Coryza Cough Small white spots in the oral cavity (Koplik’s spots) Conjunctivitis Rash The appearance of maculopapular rash reflects the immune complex formation in the skin. It correlates with viremia and onset of adaptive immune responses. The rash starts on the face and upper back after 14 days of exposure and spreads to the entire body over the next 3 days and finally fades after 5 to 6 days indicating that Cytotoxic T lymphocytes destroy infected host cells and clear the virus. Measles antibodies also appear in the circulation around this time with IgM at day 10 and IgG at day 14. They reduce measles viral load through serum neutralization. IFN-? and IL-8 levels decrease at convalescent as cytotoxic T cells decline (Heffernan and Keeling, 2008). Immunosuppression The most important pathologic feature of measles virus is immunosuppression. Most measles-related deaths are caused by secondary bacterial and viral infections. Malnourished children with weakened immune system and vitamin A deficiency are at high risk of developing complications which include blindness, diarrhoea, bronchitis, encephalitis, ear infection and pneumonia. Patients with impaired cell-mediated immunity may not develop the rash and they are susceptible to giant cell pneumonia (Manchester and Rall, 2001) Vaccination There is no antiviral therapy for measles although medications can reduce complications. Vaccination is currently the best method to prevent the disease. The first MV called Edmonston strain was isolated in 1954 on primary human kidney cells and it was subsequently adapted to chicken embryo fibroblasts and become the progenitor for currently used attenuated live vaccines. Composition of vaccines is important to elicit long-term protective immunity but not immunologic reactions and clinically significant immunosuppression. Measles vaccine is now usually given as part of a trivalent combined vaccine, MMR which is also against mumps and rubella (Hilleman, 1999). The World Health Organization has recommended infants should have the first administration of measles vaccine at 9 to 12 months because immunity requires Th1-type response. For countries with high measles transmission, a second dose should be given at age 15 to 18 months (WHO, 2009). Vaccination campaigns are effective in promoting the use of vaccination and reducing measles deaths. Between 2002 and 2008, measles vaccination has significantly reduced 78% of measles deaths from an estimated 733 000 in 2000 to 164 000 in 2008. However, many developing countries, particularly parts of Africa and Asia, still suffer from this preventable infection due to the poor access to vaccinations and lack of facilities to properly store vaccines (Manchester and Rall, 2001). Ohtake et al (2010) has reported a spray drying method was successful to produce heat-stable measles vaccine powders. However, further tests are required to demonstrate the feasibility of these dry vaccines. Molecular epidemiology is a useful tool to monitor measles and genomic study of measles virus can provide insight in the development of new and safe vaccines (Ohtake et al, 2010). The World Health Organization is making an effort to monitor outbreaks and increase immunization coverage and hopefully can ev entually eradicate the virus in the future. Subacute sclerosing panencephalitis (SSPE) SSPE is a fatal disease caused by a persistent infection with a defected form of measles virus in the brain. The common mutated components are the matrix (M), the fusion (F) and the haemagglutinin (H) proteins. Mutations can be point mutations, deletions and biased hypermutations and are mostly found in the M gene (Gutierrez et al, 2010). SSPE has a slow progression and usually develops in an interval of 5 to 10 years after the initial infection. It is very rare. Incidence rate varies between countries but the average is about one per million. Age and sex of infected individuals can affect the frequency of SSPE. Infection before the age of 2 years is associated with higher occurrences and boys are 2 times more likely to acquire SSPE (Gutierrez et al, 2010). The development of SSPE is caused by an imcompleted eradication of MV due to inadequate cell-mediated responses caused by genetic polymorphisms (Yentur et al, 2005) and high level of IL-4 but low levels of IL-12. These cytokines favour humoral response and predispose to viral replication (Hara et al, 2006). MV enters neurons by binding to host receptors CD46 and CD9 using the F protein. It replicates inside the cells and spreads to neighbouring neurons by neurokinins synaptic receptors (Makhortova et al, 2007). In addition, sequence analysis of viral RNA showed that the virus was entered from one point and disseminate throughout the brain. The defective structural envelope proteins assist them to escape from the immune system as the mutated M, F and H proteins failed to assemble and bud out the cells. Thus, the viral particles are not recognized for many years. However, inflammatory responses are finally triggered when the virus damages the host DNA and induces apoptosis (Oldstone et al, 2004). Histological examination of the brain tissue shows evidence of widespread demyelination, infiltration of immune cells and blood brain barrier damage. Glia cells and astrocytes may be activated with increased expression of MHC class II molecules and tumor necrosis factor-?. Appearance of inclusion bodies in brain tissue is also common (Akram et al, 2008). Patients are often diagnosed based on presentation and clinical findings of electroencephalography, magnetic resonance imaging and CSF serology (Koppel et al, 1996). SSPE has four clinical stages (Table 2) and most patients died within 3 years of diagnosis (Gutierrez et al, 2010). Table 2: Clinical stages of SSPE Stage Clinical manifestations I Personality changes Behaviour abnormalities II Seizures Motor decline III Rigidity Progressive unresponsiveness IV Coma Akinetic mutism (Loss of ability to speak and move) Adpated from Gutierrez et al, 2010 Word count: 2421 excluding references and plagiarism statement. Bibliography Akram M, Naz F, Malik A et al. (2008) Clinical profile of subacute sclerosing panencephalitis. J Coll Physicians Surg Pak. 18, 485-488. Atabani SF, Byrnes AA, Jaye A et al. (2001) Natural measles causes prolonged suppression of interleukin-12 production. Journal of Infectious Diseases,184, 1-9. Bolt G Berg KB (2002) Measles virus-induced modulation of host-cell gene expression. Journal of General Virology,83, 1157-1165. Ferreira CSA, Frenzke M, Leonard VHJ et al. (2010) Measles virus infection of alveolar marcrophages and dendritic cells precedes spread to lymphatic organs in transgenic mice expression human signaling lymphocytic activation molecules (SLAM, CD150). Journal of Virology, 84(6), 3033-3042. Griffin DE (1995) Immune responses during measles infection. Curr Top Microbiol Immunol, 191,117-34. Griffin DE, Ward BJ, Esolen LM (1994) Pathogenesis of measles virus infection: an hypothesis for altered immune responses. J infect Dis, 170(Suppl 1), S24-31 Gutierrez J, Issacson RS and Koppel BS (2010) Subacute sclerosing panencephalitis: an update. Developmental Medicine Child Neurology, 52, 901-907. Hara T, Yamashita S, Aiba H et al. (2000) Measles virus-specific T helper 1/T helper 2-cytokine production in subacute sclerosing panencephalitis. J Neuroviral. 6, 121-126. Hau EC, Jorio C, Sarangi F, et al. (2001) CDw 150(SLAM) is a receptor for a lymphotropic strain of measles virus and may account for the immunosuppressive properties of this virus. Virology,279, 9-21. Heffernan JM Keeling MJ. (2008) An in-host model of acute infection: Measles as a case study. Theoretical Population Biology, 73, 134-147. Hilleman MR. (1999) Combined measles, mumps and rubella vaccines. In: Ellis RW, editor. Vacinnes, development, clinical research and approval. Human Press.197-211. Horikami SM, Moyer SA. (1995) Structure, transcription and replication of measles virus. Curr Top Microbiol Immunol, 191, 35-50. Hunt (2008) Microbiology and immunology on-line: Measles (Rubeola) and mumps virus. University of South Carolina. Available at http://pathmicro.med.sc.edu/mhunt/mump-meas.htm (Access 28 February 2011) Karp CL, Wysocka M, Wahl LM et al. (1996) Mechanism of suppression of cell-mediated immunity by measles virus. Science,273, 228-231. Kehren JCMJ, Trescol-Biemont MC, Valentin AEH, et al. (2001) Mechanism of measles virus-induced suppression of inflammatory immune responses. Immunity, 14, 69-79. Kemper C, Chan AC, Green JM et al. (2003) Activation of human CD4+ cells with CD3 and CD46 induces a T-regulatory cell 1 phenotype. Nature,421, 388-392. Koppel BS, Poon TP, Khandji A et al. (1996) Subacute sclerosing panencephalitis and acquire immunodeficiency syndrome: role of electroencephalography and magnetic resonance imaging. J Neuroimaging. 6,122-125. Lenoard VHJ et al. (2008) Measles virus blind to its epithelial cell receptor remains virulent in rhesus monkeys but cannot across the airway epithelium and is not shed. J Clin Invest, 118(7), 2386-2389. Makhortova NR, Askovich P, Patterson CE et al. (2007) Neurokinin-1 enables measles vorus trans-synaptic spread in neurons. Virology. 362, 235-244. Manchester M Rall GF. (2001) Model systems: Transgenic mouse models for measles pathogenesis. Trends in Microbiology, 9(1), 19-23. Marittila J, Hinkkanen A, Ziegler T, et al. (2001) Cell membrane-associated measles virus compoents inhibit antigen processing. Virology, 279, 422-428. Moss WJ Griffin DE (2006) Global measles elimination, Nature Reviews Microbiology, 2(12), 900-908. Available at http://www.nature.com/nrmicro/journal/v4/n12/box/nrmicro1550_BX1.html (Accessed 28 February 2011) Moss WJ, Ota MO, Griffin DE. (2004) Measles: immune suppression and immune responses. The international Journal of Biochemistry Cell biology, 36, 1380-1385. Moss WJ, Ryon JJ, Monze M et al. (2002) Differential regulation of interleukin (IL)-4, IL-5, and IL-10 during measles in Zambian children. Journal of Infectious Diseases, 186, 879-887. Naniche D, Yeh A, Eto D, et al (2000) Evasion of host defenses by measles virus: wild-type measles virus infection interferes with induction of Alpha/Beta interferon production. Journal of Virology, 74(16), 7478-7484. Niewiesk S, Ohnimus H, Schnorr JJ et al. (1999) Measels virus-induced immunosuppression in cotton rats is associated with cell cycle retardation in uninfected lymphocytes. Journal of General Virology, 80, 2023-2029. Ohtake S, Martin RA, Yee L et al. (2009) Heat-stable measles vaccine produced by spray drying. Vaccine, 28, 1275-1284. Oldstone MB, Lewicki H, Thomas D et al. (2004) Measles virus infection in a transgenic model: virus-induced immunosuppression and central nervous system disease. Cell, 98, 629-640. Patterson JB, Thomas D, Lewicki H et al. (2000) V and C proteins of measles virus function as virulence factors in vivo. Virology,287, 80-89. Sato H, Kobune F, Ami Y et al. (2008) Immune responses against measles virus in cynomolgus monkeys. Comparative Immunology, Microbiology Infection Diseases, 31, 25-35. Schneider-Schaulies S, Bieback K, Avota E et al. (2002) Regulation of gene expression in lymphocytes and antigen-presenting cells by measles virus: consequence for immunomodulation. Journal of Molecular Medicine, 80, 73-85. Servet-Delprat C, Vidalain PO, Azocar O et al. (2000) Consequences of Fas-mediated human dendritic cell apoptosis induced by measles virus. Journal of Virology, 74, 4387-4393. Takeuchi K, Kadota S, Takeda M et al (2003) Measle virus V protein blocks interferon (IFN)-alpha/beta but not IFN-gamma signaling by inhibiting STAT1 and STAT2 phosphorylation. Federation of European Biochemical Societies, 545 (2-3), 177-82. Von Pirquet C. (1908) Dasverhalten der kutanen tuberculinreaktion wahrend der masern. Dtsch Med Wochenschr, 30, 1297-1300. Weidmann A, Maisner A, Garten W et al. (1999) Proteolytic cleavage of the fusion protein but not membrane fusion is required for measles virus-induced immunosuppression in vitro. Journal of Virology, 74(4), 1985-1993. World Health Organization (2009) Measles: fact sheet, WHO media center. Available at http://www.who.int/mediacentre/factsheets/fs286/en/index.html (Accessed 28 February 2011) Yanagi Y, Takeda M and Ohno Shinji. (2006) Measles virus: cellular receptors, tropism and pathogenesis. Journal of General Virology. 87, 2767-2779. Yentur SP, Gurses C and Demirbilek V et al. (2005) Alterations in cell-mediated immune response in subacute sclerosing panencephalitis. J Neuroviral, 170, 179-85. How to cite Pathogenesis of measles virus infection, Essay examples Pathogenesis of measles virus infection Free Essays string(86) " cases of autism did not increase at the period of administration of the MMR vaccine\." Introduction The development of the measles virus in earlier childhood is still relatively commonplace today in lower economic countries. A vaccination was developed approximately 40 years ago which reduced the incidence of the virus Worldwide. Unfortunately the virus has not been entirely eradicated, and a higher rate of infection still occurs more frequently in developing countries. We will write a custom essay sample on Pathogenesis of measles virus infection or any similar topic only for you Order Now In 2006 an invention of strategies were put into place by the World Health Organisation (WHO)/United Nations Children’s Fund (UNICEF)for the reduction of measles mortality rates1,2. Eradication of the measles virus encounters considerable imposing obstacles, including the growth in populations, demographic difficulties and the general population’s awareness to vaccination safety3. The WHO in 2012 plan to eradicate measles virus in the Western Pacific, a well designed sustainable plan is an necessity for this to ensure achievement, another decisive influence in the successfulness of the immunisation project is identifying the appropriate age at which immunisation should occur at. One of the main approaches to eradication of the measles virus infection is to immunise approximately 95% of the population, subsequently the majority of the population is acutely immunised against the measles virus infection which can cause astounding complications1. Infection and Spread Initial immunity for the neonate is maternal immunity transferred during pregnancy from mother to foetus. Younger women are being vaccinated in developing countries; consequently their own natural immunity is lower in comparison to non vaccinated women800. The measles virus is a contagious infection. The measles virus is caused by RNA viruses, which belongs to the genus Morbillivirus. Spread of the virus occurs due to coughing, sneezing, and personal contact with the infected. The measles virus can remain in an active state up to two hours once airborne or on contaminated surfaces. Prior to the characteristic rash associated more commonly with the measles virus, spread of the virus can develop from up to four days prior to first signs of infection and even up to four days after initial first signs of characteristic rash801. The initial symptoms of the virus display characteristics from 8-12 days following infection802. Measles virus spread is achievable through susceptible individual s whose immune system is in a state of compromised condition. Initial spread is initialised through the airways. Replication of the measles virus (MV) is acquired through numerous organs and tissues. Various types of cells and tissues are affected, which include dendritic cells (DC), and B and T lymphocytes. Generally the patient’s own immune system fights the infection and generates a life term of immunity against the infection and reoccurrence. The MV is characterised as an RNA envelope virus. Viral RNA continues to infect after initial 20 days after infection clearance. An indication of measles virus is a rash which manifests itself after approximately 10 days. Measles rash is an indication of the adaptive immune system responsiveness. At this stage CD4+ and CD8+ T cells infiltrate site for clearance. Both lymphocytes activate at same time, but CD8+ T cells is more severe, CD4+ response is longer. A diagnostic serum test for presence of IgM can be taken at this stage t o evaluate the prognosis of measles. Antibody specific IgG is also produced at this interval. The immune system experiences prolonged immunosuppression. Differential amounts of cytokines and chemokines are produced at the varied stages of infection. After the initial infection levels of IL-8 increase, IFN-? and IL-2 are elevated by activation of CD4+ and CD8+ T cells during features of a rash. Following rash exposure CD4+ generates interleukin IL-4, IL-10, and IL-13. Failure to eliminate measles infection can contribute in the development of inclusion body encephalitis and pneumonia. Subacute sclerosing panencephalitis (SSPE) can also develop from persistent infection exposure in young children203. Symptoms The measles virus presents itself as a collaboration of symptoms, which are deemed characteristics of the virus and its associated effects on the patient’s body and immune- suppressed system. Measles virus is considered a highly infectious disease. If the measles virus is persistent in the body, the virus can affect the central nervous system (CNS). Initial symptoms of the measles virus include a state of fever, coughing and a rash with small bumps. One of the main complications of persistent measles virus is the influence on the CNS40. The virus conforms to a number of characteristics. These characteristics include such signs as a fever, redness of the eyes with the most common feature being a rash on the skin41. Other symptoms of the virus include such features as coughing, muscle pain, runny nose, spots inside of mouth (Koplik’s spots), light sensitivity and eye irritation. The trade mark rash usually starts at the top of the body and moves down systematically41a. Diagnosis of acute measles include serum based specific IgM EIAs42. In 2000 a uniformed quality assured system was introduced by the World Health Organisation (WHO). The WHO established LabNet to create a homologous system to ensure diagnosis of measles and rubella. Laboratory Network (LabNet) is available in over a hundred countries. One major hurdle in the successfulness of diagnosis; is the collecting of the serum samples. Newly devised methods of sampling specimen included dried blood spots (DBS) and oral fluid (OF). Serum sampling is considered to quintessential standard for diagnosis but successful alternatives are being sought, which include the promising DBS and OF. These DBS and OF diagnostic tests offer viable potential in diagnostics for measles. Transport considerations would be less tedious when not using serum samples and the issues surrounding the safety and necessity of using needles would be eliminated. Great number of research is being implemented into more effectiv e and conclusive methods for the diagnosis of measles43. As the WHO has implemented plans to eliminate measles, greater attentiveness to the diagnostics of measles is essential and required for the WHO to be successful in their plan for reduced mortality rates44. Complications of the measles virus have been attributed to autism in children after they have received the mumps, measles, and rubella vaccine (MMR). Studies conducted suggest that the cases of autism did not increase at the period of administration of the MMR vaccine. You read "Pathogenesis of measles virus infection" in category "Essay examples" Variation in different types of autism is being studied in comparison to administration of the MMR vaccine45. The link between MMR vaccination and autism is unauthenticated but cases could exist if the child was genetically predisposed after receiving the vaccination. The vaccine is significant, as without it mortality rates would prevail46. Vaccination The implementation of vaccinations against the measles virus has been one of the most successful vaccinations worldwide. The measles vaccine has saved millions of lives around the world. It has been estimated that approximately 30-40 million people of cases of the virus each year still occur with approximately 800,000 deaths a year being contributed to the virus. The susceptibility to the measles virus is directed towards numerous influential contributory factors. The efficacy of the vaccine is dependent of a number of influential factors. Transfer of maternal antibodies occurs through the placenta. The rate of maternal antibodies in less developed countries has been shown to be lower than transferred maternal antibodies in developed countries. One contributory factor is malaria placenta infection. It has been documented that maternal antibodies still are transferred, but these antibodies tend to diminish at a greater rate. An implementation plan of action was the introduction of malaria netting which may improve the outcome. Low birth weights are more vulnerable to measles virus than normal healthy weight births. Suggestions put forward mitigate plans to vaccinate the more susceptible at an earlier age. Due to near elimination of naturally occurring measles, most immunity is due to vaccination, fewer antibodies get passed through placenta to the foetus, therefore the foetus immunity to measles is lower. Another suggestion to improve vaccination rate success is to vaccinate pre- adolescence to increase antibody levels. Finding a suitable age of vaccination is paramount and difficult, as vaccinated mothers pass on fewer antibodies than mother who naturally incurred the measles virus. An established immunisation programme has to be introduced which embraces all age groups and range of immunity. Due to lower antibody levels being transferred from the mother, the measles virus susceptibility could be as low as 4-5 months for the child. Due to such a young age of susceptibility, new regimes will have to be adapted to incorporate capturing of the earlier infected age group. The number of doses required and the efficacy of the doses is also of concern. Some countries have adopted a two dose strategy and other countries have a one dose strategy. The World Health Organisation (WHO) recommends a two dose strategy200. The different strains of the vaccines allows for different groups to be immunized. Non-injectable vaccine for the measles virus is being studied. Aerosol vaccine is displaying promising results. A study is presently on going to determine the sufficiency of aerosol vaccine in comparison to the injectable vaccine. Aerosol vaccine promises great expectations, allowing greater immune response for children 9 months or older. Aerosol vaccine allows for self administration, are less audacious to use than the injectable vaccine201. A needle-free approach is being investigated, which would prove to be cost effective and an alternative to the injectable vaccine202. A needle- free approach may be one of the better options going forward as there are numerous constraints of the live attenuated vaccines (LAVs), which include qualified administrators of vaccinations, sterile needles, and correct storage of vaccines. Non needle vaccines could allow for lower costs for administrating, easily administrated, little maintenance, one dose vaccine, safe and globally effective and availa ble.203 Subacute sclerosing panencephalitis Subacute sclerosing panencephalitis (SSPE) is contributed to the association of the measles virus. SSPE is a fatal neurological infection affecting the central nervous system (CNS), which mainly affects children. As the disease progresses, oligodendroctyes, astrocytes and endothelial cells become affected, this ultimately accumulates to death of the patient. The occurrence of SSPE was once considered to occurs in approximately 1:300,000, but more recent research would suggest cases of 1:10,00055. The direct cause of SSPE is still unidentified56 Thepathogenesis of Subacute sclerosing panencephalitis is still undefined but the incidence is considered to be mainly an adaptive immune response which involves cell- mediated responses and antibody- mediated responses, but some research suggests that both the innate and adaptive immune response is involved57,58. SSPE can linger for a number of years while causing neurological damage. Signs of SSPE become evident 6 years post measles infection. It has been documented that 95% of patients with Subacute sclerosing panencephalitis will die within 5 years of initial determination of the disease, and with only 5% of patients going into remission. The treatment Subacute sclerosing panencephalitis includes the controlling of seizures. Diagnoses of Subacute sclerosing panencephalitis are associated with electroencephalography. Demyelination and the prevalence of the measles virus are involved with SSPE. Some treatment trials are ongoing and include such drugs as isoprinosine57. Symptoms of Subacute sclerosing panencephalitis include changes in behaviour, reduction in mental capacity and involuntary twitching. Symptoms can also be represented by non conforming characteristics, which can cause SSPE to be a missed diagnosis59. Subacute sclerosing panencephalitis has also been documented to be more prevalent in males60. Future treatments for Subacute sclerosing panencephalitis include optimising the use of antivirals and molecule inhibitors61. The administration of alpha-interferon could increase the rate of mortality among patients of SSPE62. Combination therapy has been utilised in hoping to achieve the best treatment approach available, IFN-alpha and ribavirin has been optimised but with minute improved outcome63. Other research has been conducted based on apoptosis (programmed cell death) and Subacute sclerosing panencephalitis, again combination drug therapy optimising flupirtine and antiviral drugs has been acknowledged64. The aetiology of Subacute sclerosing panencephalitis is unknown, but is contributed to the relentless measles virus65. The measles virus is attributed to an array of neurological diseases66. With advancing new methodologies being discovered, advancing research and improvements directed towards disease diagnosis into SSPE, new treatments and preventative measures a viable cure may one day may become notably and genuinely palpable67. Conclusion Measles virus is contagious and affects impoverished countries more readily than developed countries. Alternative therapies focus on the influential factors which may determine susceptibility, such as deficiency in vitamin A. Measles virus in children with vitamin A deficiency may prove more harmful. The World Health Organisation set a recommendation of the required dosage of vitamin A for children with the measles virus living in impoverished surroundings30. Treatments for the contagious measles virus include vaccinations. Newly improved methods of vaccine administration are being developed, enhancing the cost- effectiveness and ease of use. The consequences of MV include Subacute sclerosing panencephalitis (SSPE), pneumonia and inclusion body encephalitis. Preventable measure and characteristic features of the virus should be dispensed to the public to educate the people on the importance of vaccination against measles virus. Reduction of two-thirds of deaths of the under-five is planned by the World Health Organisation, in its plan referred to as the Fourth Millennium Development Goal (MDG 4) by 2015. Elimination of the virus is being benchmarked against getting pre-puberty women vaccinated and aiming to vaccinate children at a younger age. Global recognition around the world on the severe consequences of the virus is essential for the eradication of this preventable infection. Countries around the World must be capable of alerting the ir appropriate agencies if a measles outbreak is thought to have occurred, failure of recognition could be detrimental to the more suscepitable31. A global uniformed approach to dosage to the young should be widely implemented around the World, and the consequences of a measles outbreak should be made clear to leading government agencies to cascade to their appropriate teams of experts. How to cite Pathogenesis of measles virus infection, Essay examples Pathogenesis of measles virus infection Free Essays Introduction Often dismissed in the developed world as a common childhood infection, measles are in fact a worrying contributor to childhood morbidity and mortality worldwide. In the UK alone, approximately 10% of cases result in complications requiring hospitalisation, 1 in 5,000 could be fatal [1]. This is much higher for the developing world where infection spreads rapidly in children that are living in close quarters, are malnourished and unable to avail of the vaccine. We will write a custom essay sample on Pathogenesis of measles virus infection or any similar topic only for you Order Now In 1994, under the national schools vaccination campaign all school children aged 5-16 were offered the mumps-measles-rubella (MMR) vaccine. An uptake of 92% under this campaign resulted in measles being all but eradicated from England and Wales [2]. Unfortunately a fall in immunisation uptake over the last decade, amid fears of a link between MMR vaccine and autism, now means that the number of susceptible children is such that measles are once again endemic in the UK [3]. Epidemics are prevalent throughout European countries including Italy, Austria Switzerland. Controlling a measles epidemic can be difficult, despite the availability of a safe and effective vaccine, as it is a highly infectious disease that spreads rapidly between susceptible individuals. Infection Spread The measles virus (MV) is single stranded RNA Morbillivirus from the paramyxovirus family that results in an acute infection of respiratory and lymphoid tissues. It is a highly contagious disease transmissible via respiratory droplets that can remain viral on surfaces for up to two hours [1]. Although it’s spread via the respiratory route and symptoms are well established little is actually known of the cellular events underlying the disease. Figure 1: Schematic diagram of measles structure [4] To better understand the process of infection and spread we must take a closer look at the measles virus (MV). MV is single negative-strand enveloped RNA Morbillivirus that contains 15,894 base pairs encoding 8 proteins. As shown in figure 1 hemagglutinin (H) and fusion (F) proteins are transmembrane envelope proteins and as such their primary role is to initiate infection. Antibodies to these proteins may render the virus inactive [4]. The RNA genome is encapsidated by the nucleotide (N) protein forming a ribonucleocapsid complex which acts as the substrate for transcription and regulation [5]. The large protein (L) and phosphoprotein (P) are also associated with the ribonucleocapsid complex and hence replication and transcription. The matrix protein (M) links the ribonucleocapsid complex to the envelope proteins during virus assembly [6]. There are also two non-structural proteins, C V encoded within the P gene that act as regulators of infection by interacting with cellular pro teins. As previously mentioned binding of H to susceptible cells is an important instigating step in measles pathogenesis. Three viral receptors for H are identifiable, CD46 a low affinity protein present on all nucleated cells, an undetermined receptor on epithelial cells and SLAM / CD150, a high affinity receptor present on subsets of lymphocytes, thymocytes, macrophages and mature dendritic cells (DCs). SLAM/CD150 is the preferential receptor for wild type strains of MV. Initially it was thought that MV infected respiratory epithelial cells which would in turn infect monocytes resulting in spread of infection to lymphoid tissues. However, this has been found not to be the case as monocytes only express CD46 low affinity receptors. Since then it has been demonstrated in vivo that lymphocytes expressing CD150 recpetors are the primary infected cells during measles in macaques [7]. However lymphocytes are not commonly found at respiratory epithelial cell surfaces hence MV target cells at transmission and throughout pathogenesis of MV are unclear. It is thought that professional antigen presenting cells (APCs) known as dendritic cells may have a dual role in mediating transmission of the measles virus [8]. Although the expected role of DCs is to capture and present MV antigens for degradation, some escape degradation and are actually protected by DCs for transportation to lymphoid tissues. Here they encounter and infect CD150+ lymphocytes allowing replication of the virus. From the primary lymphoid tissue, infected cells enter circulation. Infected peripheral blood mononuclear cells (PBMCs) are evident in the blood 7-9 days after infection [9]. From here the infection spreads to distal lymphoid tissues and to the epithelial and endothelial cells of multiple organs. Less is known about receptors used to infect these cells. There is however a number of cell surface molecules that interact with MV and as such may play an important role in MV pathogenesis, including receptor clustering, fusion, entry, cell-to-cell spread or cytokine production. These include DC-SIGN, Toll like receptor 2 (TRL2), neurokinin-1 and Fc-? receptor II. DC-SIGN (C-type lectin dendritic cell-specific ICAM-3 grabbing non-integrin) for example is credited with binding of MV to DCs. The role of which has been previously described for HIV1 [10] and has been demonstrated in MV infected macaques [7]. TRL2 interacts with H envelope protein to induce interleukin-6 (IL-6) which in turn stimulates the expression of CD150. TLR2 interaction with CD46 also inhibits IL-12 production. Symptoms Measles typically have an incubation period of 7-14 days. During the prodrome period of day 4-7 characteristic clinical symptoms of measles appear which include fever (often 104Â °F), cough, conjunctivitis and photophobia. Koplik spots, which are white buccal opposite the first and second upper molars, appear 2-3 days later followed by the maculopapular rash that lasts on average of 3-5 days [11] The rash is a manifestation of the adaptive immune response, and marks the start of viral clearance. Activated T cells and MV specific antibodies are present in circulation at this time and CD4+ and CD8+ cells have infiltrated sites of virus replication. Immunocompetent individuals will be successful in clearing the virus from these sites of replication and confer life long immunity to re-infection. Interestingly, MV appears to have a contradictory effect on the immune system with acute infections predominantly linked to periods of transient immunosuppression, often lasting weeks after the disappearance of characteristic symptoms [8]. It is these periods of immunosuppression that leaves an individual susceptible to many associated secondary complications and ultimately MV related deaths. The risk of complications may increase in densely populated areas, in children infected under the age of two, pregnant women, malnourished individuals particularly those lacking in vitamin A and in individuals who have existing immunodeficiency. Complications include respiratory complications such as bronchopneumonia and giant cell pneumonitis, neurological complications such as acute demyelinating encephalitis, subacute sclerosing panencephalitis and measles inclusion body encephalitis, gastrointestinal complications like diarrhoea or clinical hepatitis and vitamin A deficiency which may manife st as xerophthalmia a leading cause of blindness worldwide [1]. The mechanisms that result in immunosuppression are not clearly understood but a number of methods are hypothesised. For example, there is noted decrease in the numbers of T cells and B cells during the rash which for the most part is attributed to an increase in CD95 mediated and lymphocyte apoptosis [9]. This may contribute to lymphopenia, however lymphocyte numbers generally return to normal as the rash clears. It is also thought that suppression of lymphocyte proliferation may be associated with G1 arrest of the cell cycle after infection with MV [12]. Similarly T-cell proliferation may be suppressed as a result of direct inhibitory signalling by the H and F1-F2 membrane viral complex which when in contact with a cell will delay S phase entry of T cells by several days leading to accumulation of cells in the G0-G1 cell cycle phase [9]. Yet another mechanism of immune suppression is type 2 skewing of CD4+ T-cells. During infection of APCs with MV there is marked decrease in production of IL-12, which plays an important role in T-cell production of type 1 cytokines [12]. Altered CD4+T production leads T cells that fail to proliferate. Immunosuppression is characterised by lymphopenia, defective response to new antigens and a loss in the delayed type hypersensitivity responses to recall antigens. Vaccination A combined live attenuated mumps, measles and rubella (MMR) vaccine is the vaccine of choice against measles in more the 90 different countries worldwide. [13] Since its introduction in the 1970s the MMR vaccine has proven its capability to eliminate its target diseases from a number of countries. Following a national vaccination programme it was reported in 1996 that measles had all but been eradicated from the UK [2]. The US had similar success prior to this in 1993 [13] as did many other countries. Numerous strains of the MMR vaccine are produced worldwide, many of which are derived from the Edmonston strain [14]. Four non Edmonston strains including Leningrad 16, Shanghai-191, CAM-70 and TD-97 are also in use [13]. The virus is generally cultured in chick embryo cells. Most vaccines also include a small dose of antibiotic. A number of combinations of these virus, mumps virus and rubella virus are used to produce a commercial MMR vaccine. There are five commonly used MMR vaccines on the market today including M-M-R by Merck, Morupar by Chiran, Priorix by Glaxo-Smith Klein, Trimovax by Pasteur Merieux Serums and Triviraten Berna. Current US guidelines regarding vaccination with MMR recommend first dose at 12 months and a second dose to be administered before the age of 4, leaving at least 28 days between doses [15]. One dose and two dose vaccination strategies have been tried and tested in many countries [16, 17]. Although one dose strategies may achieve as much as 85% efficacy a second dose is essential to achieve eradication. Unfortunately erroneous claims linking the MMR vaccine to autism and Crohn’s disease have led to a decline in uptake of MMR vaccine and as a result countries like the US, Germany, Austria and Italy are once again facing a measles epidemic [18]. Subacute Sclerosing Panencephalitis Subacute sclerosing panencephalitis (SSPE) is an incurable complication of measles virus that presents itself 1-15years following acute MV infection [1]. It is most common in boys who under the age of two become infected with MV and is a far less common when MV infection occurs in adulthood [12]. SSPE occurs at the rate of 10,000-300,000 in acute MV infections. A disease affecting the central nervous system (CNS), SSPE initially presents as subtle cognitive changes, progressing to overt cognitive dysfunction, motor dysfunction, seizures, organ failure and eventual death. Neurons are initially targeted but as the disease progresses infected oligodendrocytes, astrocytes and endothelial cells have also been noted. Histologically it is characterised by cellular inclusion bodies, loss of neurons, inflammation, glial activation and deterioration of the blood brain barrier [12]. High numbers of MV specific antibodies are found in both blood and cerebrospinal fluid of SSPE patients. Conclusion Little is actually known of how MV may cause SSPE and other associated MV complications. Early studies using brain biopsies of SSPE patients did however show that infected neurons were unable to release budding virus. Since then extensive sequencing of such cells have lead to the conclusion that point mutations of envelope associated genes, namely as H, M, and F, could result in defective protein expression and therefore do not allow infected neurons to complete the viral process [19]. How this impacts on the development of SSPE is unclear. 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