[3] Research from Uganda published in 2012 indicates that HIV superinfection among HIV-infected individuals within a general population remains unknown.
[1] The potential of superinfection to cause rapid disease progression depends on viral and host factors.
[3] Studies have shown that a lack of neutralizing antibodies against HIV-1 infection predisposes patients to superinfection.
[3] Additionally, the tendency of HIV-1 virions to recombine when two subtypes infect a single cell increases its susceptibility to HIV superinfection.
[3] HIV-1 virions are divided into nine subtypes, all of which are characterized by different rates of disease progression, viral load and sensitivity to assays used in detection.
[9] A weakened T-cell response against the initial virus enables the superinfecting strain to resist immune control, resulting in an increased replication rate and subsequent viremia.
[9][10] Increased viral load and a declining T-cell response enables the superinfecting strain to recombine rapidly, further decreasing immune control.
[8] These can exchange genetic material such that an RNA strand from each strain is contained in a single virion.
[8] Recombination results in a rapid increase in HIV viral diversity, causing quicker adaptations to host immune response and resistance to ART.
[8] They spread geographically through human propagation, for example CRF02_AG, which is found in west and central Africa, as well as South America.
[8] 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.
[1] This is because the viruses in initial cases were all subtypes of HIV-1, with at least a 30% difference in nucleotides in their envelope proteins that makes such superinfections easier to detect.
[2] Multiregion hybridisation assays are used to identify interclade superinfection by detecting genetic differences between parental and progeny strains.
[3] Bulk sequencing is used to amplify viral RNA to enable the identification of new phylogenetic species in a patient over time.
[14] Patients in studies have displayed a shorter lag between seroconversion and experiencing an AIDS-defining clinical condition or death.
[3] Data on the prevalence of superinfection has been gathered from case reports and observational studies, suggesting that it is underreported.
[3] Incidence rates have been reported as 0% to 7.7% annually, although this varies across populations and depends on the frequency of antiretroviral drug use, the length of the follow-up period, and the method used to detect superinfection.
[20] 2002 - First definitive study on superinfection after cases reported in IV drug users in Bangkok, Thailand.
[21] 2003 - Intraclade infection by an immune response to one strain of HIV-1 cannot prevent superinfection with a second virus from the same clade.
[21] Increasing rates of antiretroviral therapy (ART) use have led to concerns about the development of drug-resistant strains which could be transmitted through superinfection.