Loss of immune control Following initial acute HIV infection, CD8+ T-cells control viral replication and maintain it at a viral set point. Following<unk> , CD8+ T-cells lose control over replication and it deviates from the set point. The mechanism responsible for this is unknown. A weakened T-cell response against the initial virus enables the<unk> g strain to resist immune control, resulting in an increased replication rate and subsequent viremia. Increased viral load and a declining T-cell response enables the<unk> g strain to recombine rapidly, further decreasing immune control. Recombination HIV virions each contain a double-stranded RNA genome. When<unk>  occurs, cells contain two different HIV strains. These can exchange genetic material such that an RNA strand from each strain is contained in a single virion. As this progeny virion infects new cells, the RNA template transcribed by viral reverse transcriptase changes, resulting in a reverse transcript with genetic material from both parental viruses. Recombination results in a rapid increase in HIV viral diversity, causing quicker adaptations to host immune response and resistance to ART. Recombination tends to produce two distinct recombinant forms, the presence of which are used as evidence of dual infection. The high prevalence of interclade recombinants increases the likelihood of<unk>  being more widespread than reported. Circulating recombinant forms Circulating recombinant forms (CRFs) are mosaic viruses - recombinants with randomly assorted genetic material from phylogenetically distinct parental viruses. They spread geographically through human propagation, for example CRF02_AG, which is found in west and central Africa, as well as South America. CRF's account for 10% of HIV infections worldwide. There are 15 known CRFs, reported on four continents. More recombinants are likely to arise in regions with a growing HIV epidemic and where viral clades intersect, including Africa, Southeast Asia and South America. Unique recombinant forms Unique recombinant forms (URFs) are mosaic viruses that have not spread geographically. They are also reported in areas where multiple viral clades intersect. In 2004, a study by AIDS on sex workers in Nairobi, Kenya, reported URF generation in a woman initially infected with clade A, and then nine years later acquired clade C, which recombined with the initial infecting virus to form a recombinant of clades A and C that fully replaced the parental clade A virions.
HIV superinfection
Hepatitis C and HIV coinfection
Epstein–Barr virus infection
Tuberculosis in relation to HIV
HIV/AIDS
Nipah virus infection
HIV-tainted blood scandal 
Risk factors for tuberculosis