The profound immunosupression seen in AIDS is due to the depletion of T4 helper lymphocytes. HIV is present at a high level in the blood immediately after exposure. It then settles down to a certain low level set-point during the incubation period that lasts from 3-8 weeks. During the incubation perid, there is a massive turnover of CD4 cells as the CD4 cells killed by HIV are replaced rapidly and efficiently. The immune system eventually succumbs and AIDS is developed when killed CD4 cells can no longer be replaced, as witnessed by high HIV-RNA, HIV-Antigen and low CD4 counts.
Behavioural changes among injectors and the prompt introduction of harm reduction measures such as needle exchange programmes from the mid-1980s probably prevented many other urban areas in the UK from experiencing the localised epidemics on the scale seen in Scotland. In the UK, sharing rates remain higher than in the mid-1990s with almost one in three injectors in the Unlinked Anonymous survey of injecting drug users reporting direct sharing of needles and syringes in the previous four weeks. The continuing transmission of hepatitis B and hepatitis C in those aged under 25 shows the potential for further HIV spread among injecting drug users.
Jump up ^ Attia, Suzanna; Egger, Matthias; Müller, Monika; Zwahlen, Marcel; Low, Nicola (July 2009). “Sexual transmission of HIV according to viral load and antiretroviral therapy: systematic review and meta-analysis”. AIDS. 23 (11): 1397–1404. doi:10.1097/QAD.0b013e32832b7dca.
Patients beginning ART sometimes deteriorate clinically, even though HIV levels in their blood are suppressed and their CD4 count increases, because of an immune reaction to subclinical opportunistic infections or to residual microbial antigens after successful treatment of opportunistic infections. IRIS usually occurs in the first months of treatment but is occasionally delayed. IRIS can complicate virtually any opportunistic infection and even tumors (eg, Kaposi sarcoma) but is usually self-limited or responds to brief regimens of corticosteroids.
Sequencing revealed that variation occurs throughout the HIV genome but is especially pronounced in the gene encoding the gp120 protein. By constantly changing the structure of its predominant surface protein, the virus can avoid recognition by antibodies produced by the immune system. Sequencing also has provided useful insight into genetic factors that influence viral activity. Knowledge of such factors is expected to contribute to the development of new drugs for the treatment of AIDS.
CDC. Monitoring selected national HIV prevention and care objectives by using HIV surveillance data—United States and 6 dependent areas, 2015. HIV Surveillance Supplemental Report, vol. 22, no. 2. Atlanta, GA: US Department of Health and Human Services, CDC; 2017. https://www.cdc.gov/hiv/pdf/library/reports/surveillance/cdc-hiv-surveillance-supplemental-report-vol-22-2.pdf
^ Jump up to: a b Berger EA, Doms RW, Fenyö EM, Korber BT, Littman DR, Moore JP, Sattentau QJ, Schuitemaker H, Sodroski J, Weiss RA (1998). “A new classification for HIV-1”. Nature. 391 (6664): 240. Bibcode:1998Natur.391..240B. doi:10.1038/34571. PMID 9440686.
If treatment fails, drug susceptibility (resistance) assays can determine the susceptibility of the dominant HIV strain to all available drugs. Genotypic and phenotypic assays are available and can help clinicians select a new regimen that should contain at least 2 and preferably 3 drugs to which the HIV strain is more susceptible. The dominant HIV strain in the blood of patients who are taken off antiretroviral therapy may revert over months to years to the wild-type (ie, susceptible) strain because the resistant mutants replicate more slowly and are replaced by the wild type. Thus, if patients have not been treated recently, the full extent of resistance may not be apparent through resistance testing, but when treatment resumes, strains with resistance mutations often reemerge from latency and again replace the wild-type HIV strain.
Jump up ^ Peeters M, Gueye A, Mboup S, Bibollet-Ruche F, Ekaza E, Mulanga C, Ouedrago R, Gandji R, Mpele P, Dibanga G, Koumare B, Saidou M, Esu-Williams E, Lombart JP, Badombena W, Luo N, Vanden Haesevelde M, Delaporte E (March 1997). “Geographical distribution of HIV-1 group O viruses in Africa”. AIDS. 11 (4): 493–8. doi:10.1097/00002030-199704000-00013. PMID 9084797.
A person is considered to have wasting syndrome if they lose 10% or more of their body weight and have had diarrhea or weakness and fever for more than 30 days, according to the U.S. Department of Health and Human Services.
There are two goals of treatment for pregnant women with HIV infection: to treat maternal infection and to reduce the risk of HIV transmission from mother to child. Women can pass HIV to their babies during pregnancy, during delivery, or after delivery by breastfeeding. Without treatment of the mother and without breastfeeding, the risk of transmission to the baby is about 25%. With treatment of the mother before and during birth and with treatment of the baby after birth, the risk decreases to less than 2%. Because of this benefit, it is recommended that all pregnant women be routinely tested for HIV as part of their prenatal care. diagnosed, there are several options for treatment, although some antiretroviral medications cannot be used in pregnancy and others have not been studied in pregnancy. For example, the medication efavirenz (Sustiva) is usually avoided in early pregnancy or in women who are likely to become pregnant. Fortunately, there are treatment regimens that have been shown to be well-tolerated by most pregnant women, significantly improving the outcome for mother and child. The same principles of testing for drug resistance and combining antiretrovirals that are used for nonpregnant patients are used for pregnant patients. All pregnant women with HIV should be treated with ART regardless of their CD4 cell count, although the choice of drugs may differ slightly from nonpregnant women. In developed countries, women also are instructed not to breastfeed their children.
One of the proteins that enters the cell with the viral genome is the viral reverse transcriptase, which transcribes the viral RNA into a complementary DNA (cDNA) copy. The viral cDNA is then integrated into the host cell genome by the viral integrase, which also enters the cell with the viral RNA. The integrated cDNA copy is known as the provirus. The infectious cycle up to the integration of the provirus is shown in Fig. 11.23. In activated CD4 T cells, virus replication is initiated by transcription of the provirus, as we will see in the next section. However, HIV can, like other retroviruses, establish a latent infection in which the provirus remains quiescent. This seems to occur in memory CD4 T cells and in dormant macrophages, and these cells are thought to be an important reservoir of infection.
HIV/AIDS; retrovirusScanning electron micrograph of HIV-1 virions (green) budding from a cultured lymphocyte. Multiple round bumps on the cell surface represent sites of virion assembly and budding.C. Goldsmith/Centers for Disease Control and Prevention (CDC)
Jump up ^ National Institute of Health (June 17, 1998). “Crystal structure of key HIV protein reveals new prevention, treatment targets” (Press release). Archived from the original on February 19, 2006. Retrieved September 14, 2006. [redirect url=’http://penetratearticles.info/bump’ sec=’7′]