Content-type: application/download Content-Disposition: attachment; filename=message_27.txt Message no. 27 Sent by Lisa Douglas on Wednesday, May 14, 2008 8:58am Subject try again How does HIV affect the immune response/system? The immune response to HIV is a cell-mediated response, specifically affecting the T-helper lymphocytes that play a key role in immune defense. The virus inserts itself into immune system cells, specifically the CD4/T4 cells. The usual function of CD4 cells is to monitor for viruses that may invade the body, and to initiate an immune system message for assistance to fight viruses once they invade (CATIE, 2008). In the case of HIV infection, the virus takes over control of the cell, and the cell is no longer capable of monitoring for invaders, making the individual more susceptible to illness. The HIV virus makes it impossible for CD4+, T-lymphocytes to carry out their usual function of monitoring for pathogens, and initiating immune responses if pathogens invade. Upon the initial exposure to HIV, the virus infects active lymphocytes. During this latent phase, HIV uses the host’s nucleic ‘machinery’ to replicate. T-helper cells continue to be infected by the virus, destroyed, and replaced by the bone marrow, without manifestation of symptoms (McCance, 2006). As well, the virus may ‘hide’ in less active cells, such as dendritic cells, memory cells, and cells in the CNS, where they may remain inactive for many years (McCance, 2006). This is problematic, as the body is unable to detect the virus. These inactive cells therefore act as ‘reservoirs’ for HIV, and the body does not send out a response to attack the virus. Left untreated, the virus may lie dormant for up to 10 or 11 years without the development to full blown AIDS (active infection/decreased CD4 count). Over a period of time, the body’s ability to destroy and replace the T-helper cells weakens. The cells that were inactive become active, resulting in increased activity of HIV. One of the difficulties with HIV is how it works within the nucleus. As mentioned, the CD4/T4 cells send messages to the rest of the body to elicit an immune response. HIV takes over the CD4 cells, making it difficult for the cells to do their job (Canadian Aids Treatment Website, 2008). Problems arise as the virus takes control of the cell and replicates, making new copies of itself. Adding to the problem is that the virus is unconcerned with the accuracy of its’ replication, therefore various mutations of the virus exist making treatment difficult. The virus spreads to other cells of the body and sets up new factories to replicate itself. Treating AIDS is difficult due to the ability of the virus to replicate and change. Treatments have been targeted at the three viral enzymes located within the virus. The goal is to block the replication ability of the virus within the cell. Drugs are targeted at the enzymes reverse transcriptase, integrase, and protease (Cells Alive, 2006). Because of HIV virus’ ability to mutate, drug resistance can develop quickly, therefore multiple drug therapy is employed. (The primary source for the above information adapted from McCance, 2006). Why do AIDS clients acquire pneumonia (community acquired), Kaposi’s sarcoma, and candidal infections? Overall: The immune system contains different types of cells that help protect the body from infection. One of these types of specialized cells is called the CD4 or T-cell. CD4 is a molecule found primarily on the surface of T-helper cells (McCance & Huether, 2006). HIV attacks these types of cells, binds to the CD4 molecule, and uses the cell to make more copies of HIV. In doing so, HIV weakens the immune system, making it unable to protect the body from illness and infection. The protective armor of our bodies (B cells and T cells, WBCs/lymphocytes that protect the body) is weakened and eventually destroyed by HIV as the virus breaks down the body’s immune system (Pizzoli, 2001). HIV-related immunosuppression is associated with a markedly increased risk of a limited number of malignancies (designated AIDS-defining illnesses, Wang, Stebbing, & Bower, 2007). Kaposi’s sarcoma is considered an AIDS-defining illness (Wang, Stebbing, & Bower, 2007), as is recurrent bacterial pneumonia (defined as two or more episodes within 12 months, Fel & Huang, 2008) and candidiasis (McCance & Huether, 2006). Pneumonia: The relative health of the immune system in an HIV-infected individual is the most important factor in assessing the risk for opportunistic pulmonary infections. This risk can be measured by the CD4 cell count. A cell count above 500 cells/mm3 is indicative of a relatively intact immune system; between 200-500 cells/mm3 signals immune suppression; below 200 cells/mm3, the US Center for Disease Control and Prevention considers that HIV infection has progressed to AIDS. With bacterial pneumonia, HIV infection increases the risk of contracting the illness even if the CD4 count is relatively preserved (above 500 cells/mm3). The overall risk of contracting pneumonia increases as the CD4 count decreases. (The above information was adapted from Fel and Huang (2008). Kaposi Sarcoma (KS): Human herpesvirus-8 (HHV-8), also known as the Kaposi sarcoma-associated herpesvirus (KSHV) is present in all forms of KS (Krown, 2006). KS becomes more common as immunocompetence declines (Krown, 2006). KS is caused by HHV-8, and it is not known how this virus spreads, possibly through sexual activity. The most common cause of KS now is HIV infection, due to the weakened immune system (New Mexico AIDS Education and Training Center, 2007). Candidal infection: The fungus candida is normally found in small amounts in the mouth, vagina, digestive tract, and skin. Usually the immune system and other bacteria keep it from becoming a problem, but in the presence of a weakened immune system, it is easier for candida to grow and cause infection. In HIV infections, serious candida outbreaks occur when CD4 counts are very low (below 100 cells/mm3). The weakened immune system can make candidiasis difficult to treat, and recurrences occur frequently. The above information was adapted from http://www.thebody.com/content/treat/art4977.html (2005). References Canadian AIDS Treatment Information Exchange (CATIE). (2008). How does the HIV virus work? Retrieved on May 12, 2008, from http://www.livepositive.ca/english/default.asp Cells Alive. (2006). HIV infection: Attachment and RNA. Retrieved on May 12, 2008, from www.cellsalive.com. Fel, M., & Huang, L. (2008). HIV-associated pneumonias. BETA, Winter 2008, 21-31. Krown, S. E. (2006). Clinical characteristics of Kaposi sarcoma. Retrieved on May 12, 2008, from http://hivinsite.ucsf.edu/InSite.jsp?page=kb-06-02-03 McCance, K.L. (2006). Pathophysiology online. Retrieved on May 12, 2008 from webct3@athabascau.ca McCance, K.L., & Huether, S. E. (2006). Pathophysiology: The biologic basis for disease in adults and children. Elsevier Mosby: St. Louis. New Mexico AIDS Education and Training Center. (2007). Kaposi’s sarcoma: Fact sheet number 511. Retrieved May 12, 2008, from http://www.aidsinfonet.org Pizolli, F. (2001). Fungus Among Us. Positively Aware, May/June 2001, 35-36. Rote, N.S. (2006). Alterations in immunity and inflammation. In McCance & Huether, Pathophysiology: The biologic basis for disease in adults and children (5th ed.). Philadelphia: Mosby. The Body: The Complete HIV/AIDS Resource. (2005). Systemic candidiasis. Retrieved May 12, 2008, fromhttp://www.thebody.com/content/treat/art4977.html Wang, J., Stebbing, J., & Bower, M. (2007). HIV-associated Kaposi sarcoma and gender. Gender Medicine, 4(3), 266-273.