Le to PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/28388412 identify five cases of dual infection by studying only one genomicSoares de Oliveira et al. Virology Journal 2012, 9:223 http://www.virologyj.com/content/9/1/Page 6 ofFigure 3 Phylogenetic tree constructed using a maximum-likelihood method from pol-IN (219 bp ; nt 4269?488 of HXB2) fragments from five PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/28827318 of the samples isolated from MSM observed to be infected with both subtype B (indicated by black circles) and subclade F1 DNA (indicated by black squares) along with HIV-1 reference sequences from the Los GSK343MedChemExpress GSK343 Alamos HIV-1 database representing 11 genetic subtypes. For purposes of clarity, the tree was midpoint rooted. The approximate likelihood ratio test (aLRT) values of 70 are indicated at nodes. The scale bar represents 0.05 nucleotide substitutions per site.region of the HIV genome, similar to the Kenyan study [38]. In the Kenyan study, the authors observed seven cases of HIV-1 superinfection among 36 high-risk women and only five cases of superinfection were detected bydifferences in only one gene. Unexpectedly, a lack of detectable HIV-1 dual infections has recently been reported in a retrospective study of 83 samples from chronically infected patients on antiretroviral treatment throughoutSoares de Oliveira et al. Virology Journal 2012, 9:223 http://www.virologyj.com/content/9/1/Page 7 ofthe KwaZulu-Natal region that has a high HIV prevalence [40]. The lack of dual infections in this study was explained by the ability of the immune system to evolve overtime to eliminate or prevent a second viral infection during chronic infection [40,41]. Despite a large body of literature, the true prevalence and the timing of immune selection in HIV co/superinfection cases have not yet been substantiated by robust clinical studies and the limited data that do exist have yielded inconclusive or contradictory findings that partially contribute to the controversies surrounding the challenge and implications of HIV co/superinfection for efficient vaccine design [38,42,43]. Our estimates of subtype B and F1 dual infection rates are not directly comparable to other published studies as each study group has used different research designs, methodologic approaches, and different target population for the search of different HIV-1 subtypes [8,16,44-52]. All together, these data lend further support to the conclusions that dual infections are an integral part of the HIV/AIDS epidemic, particularly in countries where multiple subtypes are circulating in the population [15]. In summary, our data adds to the knowledge of the prevalence of HIV-1 dual infections caused by HIV-1 subtype B and F1 viruses in MSM subjects and provides data from a country where such a phenomenon is rarely documented. Furthermore, these data agree with the consensus that the presence of two or more HIV-1 subtypes within an infected individual is relatively frequent [53,54]. Thus, testing for co-infection and superinfection and the implementation of effective preventative measures in the MSM population remains relevant issue.Competing interests The authors declare that they have no competing interests. Authors’ contributions ACSO, RPF, ACC and SSS conceived and designed the study, performed the experiments analyzed the data and wrote the paper. MMS collected clinical data, KCB, SMSO, PRC, CT, and HTIT contributed reagents/materials/analysis tools. ECS EGK and SSS critically reviewed the paper and secured funding. All authors read and approved the final manuscript. Acknowledgements.
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