Modes of Transmission of HIV, HBV and HCV - Research Paper Example

Modes of Transmission of HIV, HBV and HCV Introduction Governments all over the world are trying to fight the current pandemic of HIV infection which is soaring to new heights each year. The infection has not only caused significant mortality and morbidity; it has also drained the countries financially owing to the cost involved in research, investigation, treatment, evaluation and awareness. According to the WHO, there are more than 38 million HIV infection cases globally (Dubin, 2007). There is no cure for infection with HIV and there is no vaccine either. There are 2 other viruses which cause chronic infection and have no cure. They are HBV and HCV. There is an effective vaccine for HBV and this has caused decrease in the number of cases in the world. The only hope for control of these infections remains in identifying the modes of transmission and education people about measures to prevent transmission. The following essay elaborates the various modes of transmission of these viruses with a brief flip through the pathogenesis. The pathogenesis of HIV, HBV and HCV infections Human Immuno Deficiency Virus or HIV is a type of retrovirus that falls into the sub group of slow-virus or lentivirus. Viruses belonging to this subgroup of retrovirus are characterized by long latent period, viremia, disruption of proper immune responses and infection of the central nervous system (Dubin, 2009). HIV is a spherical virus. The core consists of a capsid which encloses 2 copies of single-stranded RNA and important enzymes like proteases, reverse transcriptase, ribonuclease and integrase. The capsid is made up of viral protein p24 and is covered by a matrix which is made up of viral protein p17. The matrix is surrounded by a phospholipid- envelope consisting of the proteins Env and glycoproteins, gp120 and gp41. The RNA genome has nine genes of which gag, pol and env are very important to make new structural proteins. The pathogenesis of HIV infection depends on the life cycle of the virus, the cellular environment of the host and the number of viruses in the infected host. The severity and rate of progression of the disease depends on the virulence of the virus strain, co-infection with other viruses or bacteria, age of the host and the genetic factors of the host. HIV virus specifically affects monocytes and CD4 T lymphocytes. Other cells which possess the CD4 receptor like tissue macrophages, natural-killer cells, dendritic cells, hemopoietic stem cells, T and B lymphocytes, endothelial cells, gastrointestinal epithelial cells and microglialcells may be affected. Probability of infection in an individual who is exposed to HIV virus is dependent on 2 factors: the number of infective virions in the body fluid that has come in contact with the individual and the number of CD4 cells that have come in contact with these viruses (Dubin, 2009). After coming in contact with CD4 receptors, the viruses enter the cells and replicate to produce more virions which are released into the blood stream by surface budding or lysis of the host cells. These virions come in contact with new host CD4+ cells and the infection thus continues and spreads. The viruses get trapped in follicular dendritic cells or FDCs which become a reservoir for the viruses. Viruses in FDCs are infectious even when coated with antibodies. Other important reservoirs of infection are macrophages and monocytes. New immune processes in the body of the host like release of cytokines can activate the CD4+ lymphocytes and increase the susceptibility of the cells to the infection. There are many ways by which the virus kills the host. When large amounts of viruses are produced in the cells, direct killing occurs due to disruption of the cell membrane and interference with cellular machinery. Syncytia formation with adjacent uninfected cells can result in the death of uninfected cells. Distortion of cellular regulation by the virus can result in apoptosis of the host cell. Binding of HIV to the cell surface of uninfected cells can make them targets for destruction by Killer T cells (Dubin, 2009). HIV is carried to other parts and organs of the body through macrophages and monocytes which seldom get killed after infection (Dubin, 2009). Hepatitis B virus or HBV is a species categorized under genus orthoviridae which falls into the family Hepadnaviridae. Viruses from this family have an affinity mainly to liver cells and also to cells of the kidney and pancreas and mononuclear cells. The HBV particle consists of a nucleocapsid core and an outer envelope. The core is icosahedral and is made up of proteins and the envelope is made up of lipid. The core has viral DNA which is circular and also DNA polymerase. The enzyme also has reverse transcriptase activity. The significant antigens present in the virus are HBsAG or the surface antigen, HbcAg or the core antigen, HBV DNA polymerase. HBeAg is a part of HBcAg (WHO, 2009). HBV causes various pathologies in the body. It can cause acute hepatitis, chronic carriage, chronic hepatitis and cirrhosis, and hepatocellular carcinoma (WHO, 2009). After entering the host body, the HBV binds to a cell surface receptor and enters the cell by endocytosis. This is known as attachment. After this, the membrane of the virus fuses with that of the host cell and releases core proteins and mRNA. This is known as penetration. Chaperones, a type of host proteins, transfer the viral DNA to the cell nucleus where a closed circular viral DNA is formed. This is known as uncoating. New genome copies, core protein and viral DNA polymerase are done using closed circular DNA as template and with the help of mRNA of the host. This is known as replication. Replication from one template yields 4 viral transcripts which further form progenies that are either released from the cell or returned to the nucleus. This is known as assembly. Virion P protein synthesizes DNA with the help of reverse transcriptase in the cytoplasm. This is known as release (Pyrsolous and Reddy, 2009). HBV is resistant to adverse temperatures and humidity. The disease caused by the virus is not due to cytotoxicity but due to the immune responses of the host to the antigens of the virus. Thus, many HBV carriers are asymptomatic and those with immune response defects suffer from only milder forms of liver injury. The immune responses involve both CD4+ and CD8+ T lymphocytes. These activated lymphocytes are able to detect HBV-related peptides which are located on the liver cells surface. There are four stages which have been identified in the life cycle of the virus in the host. The first stage is also called the incubation period and it occurs 2-4 weeks after contracting the infection (Pyrsolous and Reddy, 2009). This stage is also known as stage of immune tolerance and the virus replicates actively without affecting the aminotransferase levels and without causing any symptoms. During the second stage of the disease, inflammatory reactions occur and even cytopathic effects are seen. In this stage, it is possible to identify HBeAg in the sera. At the same time, the HBV DNA levels will decline. This stage lasts for about 3- 4 weeks during which time, the patient manifests symptoms (Pyrsolous and Reddy, 2009). For those which chronic infection tendency, this stage may last for as many as 10 years (Pyrsolous and Reddy, 2009). The third stage constitutes of targeting of the HBV and infected hepatocytes by the host immune system. The viral genome integrates with the hepatocyte genome of the host. The virus does not replicate any more. In this stage, HBeAb is detectable, suggestive of immune response by the host. The HBV DNA levels fall to minimum or undetectable ranges. Serum aminotranferase levels continue to be within normal limits. HBsAg is detectable. In the last stage, the body produces antibodies to all the antigens of the virus. The virus is not detectable (Pyrsolous and Reddy, 2009). Hepatitis C Virus or HCV is a member of the genus hepacivirus which belongs to the family Flaviviridae. The virus is small and spherical in shape. It contains a central genome made up of a single stranded RNA which is enclosed by the capsid proteins. . The outer part of the virus is made up of an envelope. The main structural proteins of the virus are core protein and a couple of envelope proteins called glycoproteins E1 and E2. The virus also contains non-structural proteins like proteases, helicase and RNA-dependent polymerase which are necessary for the life cycle of the virus in the host. HCV virus mainly affects the liver. After entering the host, the virus reaches the liver cells and enters them through surface molecules. Once, inside the cell, the virus releases the genetic material to start replication. The viral genome acts as a template for the synthesis of negative strand and then this becomes a template for further synthesis of positive strand. Structural and non-structural proteins are also synthesized and assembled with the genetic material to form virions. HCV mainly causes clinically inapparent infection. Chronic infection occurs only in those who are immunocompromised and can culminate in fibrosis and cirrhosis of the liver. The exact mechanism by which the virus causes the disease is not yet clearly identified. The virus triggers both humoral and cellular immune responses (Liang, et al, 2000). HCV is basically noncytopathic like HBV and the pathogenesis is mainly caused by the immunological response of the host to the virus. The onset of liver disease and viral clearance coincides with the CD8+ T cell response and also the presence of HCV-specific T cells in the liver. The immune response occurs after several weeks after infection. Type-1 interferon is strongly induced by the virus, but it does not help in the clearance of the virus. However, absence of HCV-specific T-cell response in the liver and decreased production of interferon-1 in the setting of low viremia is associated with persistent uncontrolled infection (Liang, et al, 2000). Transmission of HIV, HBV and HCV infections The most common mode of transmission of HIV is through sexual contact with the infected person. Infact, this mode of transmission accounts for nearly 75-85% of transmissions (Royce et al, 1997). Globally, the infection is transmitted mostly through heterosexual men and women when compared to homosexual men and women (Dubin, 2009). However, in the US, especially amongst men, most of the HIV infections are acquired through homosexual contact (Greenwald et al, 2006). The glandular epithelium of the transformation zone in the cervix of the women harbors HIV in infected cases (Royce et al, 1997). Spread through sexual contact depends on a number of factors. Studies have shown that individuals with CKR5 mutation are resistant to HIV infection. Those in the late stages are in a position to spread the disease much ore than those who are in early stages. It is unclear whether antiretroviral therapy or ART soon after exposure decreases the risk of infection (Royce et al, 1997). ART in the infectious partner definitely affects infectivity. Presence of reproductive tract infections and cervical ectopy makes an individual highly susceptible for contraction of HIV. Studies have shown that male circumcision has a protective effect against HIV (Royce et al, 1997). Sex during menstruation with the infected partner increases the risk of acquiring the disease. When condoms are used as a contraceptive measure, the risk of HIV transmission is decreased. Other forms of contraception have doubtful effects on the transmission of HIV (Royce et al, 1997). Other modes of transmission are unsafe needle practices and vertical transmission from mother-to-baby. After introduction of screening before blood transfusion, transmission of the disease through blood transfusions has significantly reduced. In vertical transmission, the babies may get infected in the womb, during birth, or through breast feeding. Health workers may get infected through accidental needle pricks, splashing of infected body fluids and from infected doctor /surgeon to patients. HIV does not survive well outside the human body and thus cannot spread through food, water, air or insects (Royce et al, 1997). Like in any other body fluid, the virus is present in saliva too, but only in such small concentrations that the risk of spread through kissing is minimal. Transmission though tears and sweat is also negligible. Non-sexual transmission amongst household members is rare and may occur due to contact between exposed mucous membranes and skin with blood that is infected with HIV like in sharing of razors and tooth brushes. Another important source of transmission is human bite where contact between cut mucous membranes and skin can occur. Casual contact at work place or transport or food establishments does not cause HIV (Royce et al, 1997). Beauty parlors, both of men and women are potential sources of transmission of infection if proper precautions like disposable razors and ear/nose pricking needles are taken. Incarceration is another important source of transmission of infection because it disrupts existing relationships and prompts risky sexual behaviors in and out of the jail (Wohl, n.d.) HBV is transmitted from one person to another by means of contact with infected blood and certain other body fluids like vaginal fluid and semen. The modes of transmission are similar to HIV infection, but HBV is atleast 50 to 100 times more infectious than HIV because of its ability to survive and be infectious even when outside the host body for a week or so (WHO, 2009). In the developed nations like North America and Western Europe, the most common modes of transmission are unsafe sex practices in early adulthood and intravenous drug abuse. However, the transmission is different in developing countries wherein the common transmission modes are sexual contact, blood transfusion, vertical transmission through pregnancy, intravenous drug abuse and other unsafe needle practices, and inapparent early childhood infections from parents (WHO, 2009). The virus cannot spread through casually at workplace or by water or food (WHO, 2009). At present, the predominant means of transmission of HCV virus is exposure of the skin to blood infected with the virus. Percutaneous exposure occurs in intravenous drug abuse. Another important source of transmission is blood transfusion. However, the advent of screening of blood donors for this virus has significantly decreased the risk of this mode of transmission. Acupuncture, sharing razors, tattooing and needle stick injuries in a health care setting are other causes of percutaneous exposure to the virus. According to Rischitelli et al (2001), needle stick injury may not be an important mode of transmission because the incidence of HCV in health care workers is as much as in general population. Other uncommon routes of HCV transmission are high-risk sexual activity and vertical transmission (Yeung et al, 2001). HCV does not spread through casual household contact and contact with infected saliva. Scenario in Saudi Arabia Like any other country in the world, HIV has affected Saudi Arabia in epidemic proportion. In the year 2003, 7807 cases were reported in Saudi Arabia, of which 1743 were Saudi nationals and 6064 non-Saudi individuals. Males were seen to be at more risk of the infection, with the male-female ratio being 3:1 (Al-Mazrou, 2005). About 78% of the HIV cases were adults between 15- 49 years (Al-Mazrou, 2005). Dammam, Jeddah and Riyadh accounted for 67% of the cases (Al-Mazrou, 2005). 46% of these acquired the infection through unprotected sexual activities. (Al-Mazrou, 2005). According to Mandani et al (2004), among Saudi citizens, heterosexual contact accounted for 37.9% of cases, homosexual contact- 2.5%, bisexual- 0.8%, blood transfusion-25%, perinatal transmission- 6.5%, intravenous drug abuse- 1.3% and unknown cause- 26%. Infection through blood transfusion declined to zero from 2001, due to pre-transfusion screening (Al-Mazrou, 2005; Mandani et al, 2004). While the prevalence of HIV continues to rise, HBV prevalence is declining in Saudi (Ayoola, 2003). Conclusion HIV, HBV and HCV are chronic infections with no available treatment. While HBV has an effective vaccination against it, the others have no vaccines developed so far. All the 3 viruses are acquired through contact with blood and body fluids. After entering the body, these viruses enter their target cells and multiply. While HIV causes pathogenesis through destruction of cells, the other 2 cause damage because of the immune responses of the body. All the 3 are mainly transmitted through unprotected sexual activities. Other modes of transmission are improper needle abuse, vertical transmission and blood transfusion. The advent of effective screening methods prior to transfusion has decreased transmission of these viruses through blood transfusion. References Al-Mazzrou, Y.Y., Al-Jeffri, M.H., Fidail, A., et al. (2005). HIV/AIDS epidemic features and trends in Saudi Arabia. Ann Saudi Med, 25(2), 100-104. CDC. (2007). HIV and its Transmission. Department of Health and Human Services. Retrieved on May 3, 2009 from http://www.cdc.gov/hiv/resources/factsheets/transmission.htm Dubin, J. (2009). HIV, Early Recognition and Rapid Testing. Emedicine from WebMD. Retrieved on May 3, 2009 from http://emedicine.medscape.com/article/783434-overview Ganem, D., and Prince, A.M. (2004). Hepatitis B Virus Infection — Natural History and Clinical Consequences. N Engl J Med, 350, 1118-29. Greenwald, J.L., Burstein, G.R., Pincus, J., and Branson, B. 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