"HIV-1 subtype G infects approximately 1.5 million individuals, primarily in west Africa, but also on the Iberian peninsula, Cuba and, more rarely, other global locations (Hemelaar et al., 2011). Cameroon is located in west central Africa, the epicentre of the HIV epidemic, where many HIV-1 types and subtypes co-circulate (Peeters et al., 2003; Tebit and Arts, 2011). Despite having a relatively low HIV prevalence, Cameroon has one of the most genetically diverse HIV epidemics in the world, with a very large variety of HIV-1 circulating recombinant forms (CRFs) (Brennan et al., 2008; Carr et al., 2010; Ceccarelli et al., 2012; Soares et al., 2010; Tongo et al., 2013; Torimiro et al., 2009). "
"Despite the relatively low prevalence of HIV infection when compared with other African countries, Cameroon harbors an extreme variability of circulating HIV strains. All major types (HIV-1 and -2), groups (main [M], outlier [O], non-M/non-O [N], and P), subtypes and recombinant forms have been reported almost exclusively in native Cameroonians [Simon et al., 1998; Peeters et al., 2003; Vallari et al., 2011]. CRF02_AG, a CRF derived from subtype A and Grant sponsor: European AIDS Treatment Network (NEAT); Grant number: LSHT/CT/2006/037570; Grant sponsor: European Commission Framework 7 Programme. "
[Show abstract][Hide abstract] ABSTRACT: Currently the prevalence of HIV-1 infection in Cameroon is 5.1%, CRF02_AG subtype is responsible for about 50% of infections. Since an HIV-1 drug resistance test is not yet available widely, accurate data on the prevalence of resistant viral strains are missing. The objective of this study was to determine HIV-1 genetic diversity and to characterize HIV-1 mutations conferring drug resistance among antiretroviral therapy (ART)-naïve and ART-treated patients. A cohort of 239 patients infected with HIV were followed-up between January 2007 and July 2010 in Cameroon. Two hundred and sixteen plasma samples were sequenced for phylogenetic analysis and identification of drug resistance mutations in the HIV-1 pol region. A significant genetic diversity was found: Seven pure subtypes (A1, A3, D, F1, F2, G, H), nine circulating recombinant forms (CRFs: 01_AE, 02_AG, 06cpx, 09cpx, 11cpx, 13cpx, 16cpx, 18cpx, 37cpx) and one new unique recombinant form (URF) (G/F2). The rate of transmitted drug resistance (TDR) in naïve patients was 8.2% (4/49). Around 80% of patients failing a first-line ART harbored a virus with at least one resistance mutation to two antiretroviral (ARV) classes, and 36% of those failing a second-line regimen carried a virus with at least one resistant mutation to three ARV classes. The high level of drug resistance observed in the cohort is alarming because this occurred as a result of only few years of treatment. Adherence to therapy, adequate education of physicians, and the appropriate use of genotypic resistance assay are critical points of intervention for the improvement of patient care.
Journal of Medical Virology 05/2012; 84(5):721-7. DOI:10.1002/jmv.23244 · 2.22 Impact Factor
"By analogy with HIV-1, these lineages have been termed groups A– H, although only groups A and B have spread within humans to an appreciable degree. Group A has been found throughout western Africa (Damond et al. 2001; Peeters et al. 2003), whereas group B predominates in Cote d'Ivoire (Pieniazek et al. 1999; Ishikawa et al. 2001). All other HIV-2 " groups " were initially identified only in single individuals, suggesting that they represent incidental infection with very limited or no secondary spread. "
[Show abstract][Hide abstract] ABSTRACT: Acquired immunodeficiency syndrome (AIDS) of humans is caused by two lentiviruses, human immunodeficiency viruses types 1 and 2 (HIV-1 and HIV-2). Here, we describe the origins and evolution of these viruses, and the circumstances that led to the AIDS pandemic. Both HIVs are the result of multiple cross-species transmissions of simian immunodeficiency viruses (SIVs) naturally infecting African primates. Most of these transfers resulted in viruses that spread in humans to only a limited extent. However, one transmission event, involving SIVcpz from chimpanzees in southeastern Cameroon, gave rise to HIV-1 group M-the principal cause of the AIDS pandemic. We discuss how host restriction factors have shaped the emergence of new SIV zoonoses by imposing adaptive hurdles to cross-species transmission and/or secondary spread. We also show that AIDS has likely afflicted chimpanzees long before the emergence of HIV. Tracing the genetic changes that occurred as SIVs crossed from monkeys to apes and from apes to humans provides a new framework to examine the requirements of successful host switches and to gauge future zoonotic risk.
Cold Spring Harbor Perspectives in Medicine 09/2011; 1(1):a006841. DOI:10.1101/cshperspect.a006841 · 7.56 Impact Factor
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