Both high mutation rates and recombination contribute to the genetic diversity of human immunodeficiency virus type 1 (HIV-1). Among viruses of the main group, which are responsible for the HIV-1 pandemic, 21 circulating genetic forms have been reported, 11 of which are recombinant between > or = 2 subtypes. In Western Europe and the Americas, the HIV-1 epidemic is largely dominated by B subtype viruses; however, infections with diverse non-B subtype genetic forms are increasingly being recognized. In Western Europe and North America, most of them have been identified in immigrants or travelers returning from areas with high HIV-1 prevalence, mainly from sub-Saharan Africa and Southeast Asia, where non-B subtype genetic forms predominate, but propagation within other groups has been reported in some Western countries. This may have implications for prophylactic and therapeutic strategies and, by bringing in contact different genetic forms, may favor the generation of novel recombinant viruses. Travelers from different categories--including immigrants, military personnel, seamen, tourists, expatriates, diplomats, and businessmen--may be at risk of transporting HIV non-B subtype genetic forms to Western countries.
"Many other non-B subtypes and circulating recombinant forms (CRFs) are being reported with increased travel and immigration [6–9]. Despite the known genetic diversity of HIV and the potential emergence of new variants [10,11], the impact of subtype diversity on initiation and sequencing of ART regimens, resistance mutations and clinical disease progression remains relatively unknown. "
[Show abstract][Hide abstract] ABSTRACT: There are 31 million adults living with HIV-1 non-B subtypes globally, and about 10 million are on antiretroviral therapy (ART). Global evidence to guide clinical practice on ART response in HIV-1 non-B subtypes remains limited. We systematically searched 11 databases for the period 1996 to 2013 for evidence. Outcomes documented included time to development of AIDS and/or death, resistance mutations, opportunistic infections, and changes in CD4 cell counts and viral load. A lack of consistent reporting of all clinical end points precluded a meta-analysis. In sum, genetic diversity that precipitated differences in disease progression in ART-naïve populations was minimized in ART-experienced populations, although variability in resistance mutations persisted across non-B subtypes. To improve the quality of patient care in global settings, recording HIV genotypes at baseline and at virologic failure with targeted non-B subtype-based point-of-care resistance assays and timely phasing out of resistance-inducing ART regimens is recommended.
Journal of the International AIDS Society 05/2014; 17(1):18944. DOI:10.7448/IAS.17.1.18944 · 5.09 Impact Factor
"Understanding HIV molecular epidemiology and potential future spread of different non-B subtypes has also clinical relevance. It is already known that differences among HIV-1 genetic forms may impact both the clinical management and surveillance of drug resistance, as a result of the effect of treatment on non-B HIV-1 strains [45, 46]. "
[Show abstract][Hide abstract] ABSTRACT: . The evolutionary and demographic history of the circular recombinant form CRF02_AG in a selected retrospective group of HIV-1 infected men who have sex with men (MSM) resident in Central Italy was investigated.
. A total of 55 HIV-1 subtype CRF02_AG
sequences were analyzed using Bayesian methods and a relaxed molecular clock to reconstruct their dated phylogeny and estimate population dynamics.
. Dated phylogeny indicated that the HIV-1 CRF02_AG strains currently circulating in Central Italy originated in the early 90's. Bayesian phylogenetic analysis revealed the existence of a main HIV-1 CRF02_AG clade, introduced in the area of Rome before 2000 and subsequently differentiated in two different subclades with a different date of introduction (2000 versus 2005). All the sequences within clusters were interspersed, indicating that the MSM analyzed form a close and restricted network where the individuals, also moving within different clinical centers, attend the same places to meet and exchange sex.
. It was suggested that the HIV-1 CRF02_AG epidemic entered central Italy in the early 1990s, with a similar trend observed in western Europe.
"Majority of patients carrying non B subtype strains were infected through heterosexual contact and this association was found to be statistically significant. Numerous studies have shown that non-B infections in Europe are mainly associated with heterosexual infection among immigrants or persons epidemiologically linked to sub-Saharan Africa (Gifford et al., 2006; Thomson and Nájera, 2001). In contrast to that finding, vast majority of patients in our study reported to be infected locally, with no epidemiological links abroad. "
[Show abstract][Hide abstract] ABSTRACT: Worldwide HIV-1 pandemic is becoming increasingly complex, with growing heterogeneity of subtypes and recombinant viruses. Previous studies have documented HIV-1 subtype B as the predominant one in Serbia, with limited presence and genetic diversity of non B subtypes. In recent years, MSM transmission has become the most frequently reported risk for HIV infection among newly diagnosed patients in Serbia, but very little is known of the network structure and dynamics of viral transmission in this and other risk groups. To gain insight about the HIV-1 subtypes distribution pattern as well as characteristics of HIV-1 transmission clusters in Serbia, we analyzed the genetic diversity of the pol gene segment in 221 HIV-1- infected patients sampled during 2002-2011. Subtype B was found to still be the most prevalent one in Serbia, accounting for over 90% of samples, while greater diversity of other subtypes was found than previously reported, including subtypes G, C, A, F, CRF01 and CRF02. In total, 41.3% of analyzed subtype B sequences were found associated in transmission clusters/network, that are highly related with MSM transmission route.
Infection, genetics and evolution: journal of molecular epidemiology and evolutionary genetics in infectious diseases 06/2013; 19. DOI:10.1016/j.meegid.2013.06.015 · 3.02 Impact Factor
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