Phylogenetic Analysis of HIV Type 2 in Ghana and Intrasubtype Recombination in HIV Type 2

Takehisa, Jun; Osei-Kwasi, Mubarak; Ayisi, Nana K.; Hishida, Osamu; Miura, Tomoyuki; Igarashi, Tatsuhiko; Brandful, James; Ampofo, William; Netty, Victor B.A.; Mensah, Margaret; Yamashita, Masahiro; Ido, Eiji; Hayami, Masanori

doi:10.1089/aid.1997.13.621

Cited by 18 publications

(13 citation statements)

References 12 publications

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“…All individuals but one in this study were infected with HIV-2 subtype A. This variant is the most common worldwide, except in Ivory Coast, Ghana, and Equatorial Guinea [Takehisa et al, 1997;Heredia et al, 1997;Machuca et al, 1998;CavacoSilva et al, 1998;Machuca et al, 1999], where HIV-2 subtype B is prevalent. Because these regions are not former colonies of Portugal, it was not surprising that subtype A was the most prevalent in our study population, in agreement with recent reports from Portugal [Cavaco-Silva et al, 1998;Heredia et al, 1998b].…”

Section: Discussionmentioning

confidence: 73%

“…Among the pathogenetic mechanisms contributing to the lower virulence of HIV-2, a reduced functionality of its nef regulatory gene [Switzer et al, 1998] and a low infectious virus level in infected individuals, have been suggested [Simon et al, 1993]. Six different genetic subtypes of HIV-2 (A-F) have been recognized so far, HIV-2 subtype A being the most predominant [Gao et al, 1994;Chen et al, 1997;Takehisa et al, 1997;Peeters et al, 1998]. Lower or even lack of pathogenicity have been suggested for non-A subtypes [Gao et al, 1994].…”

Section: Introductionmentioning

confidence: 99%

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Human immunodeficiency virus type 2 (HIV-2) in Portugal: Clinical spectrum, circulating subtypes, virus isolation, and plasma viral load

et al. 2000

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The human immunodeficiency virus type 2 (HIV-2) is responsible for 4. 5% of AIDS cases in Portugal. Six HIV-2 subtypes have been described so far, subtype A being proposed as more pathogenic than the rest. The relationship between the clinical status and levels of both cellular and plasma HIV-2 viraemia is not well known, nor their modifications under antiretroviral therapy. Thirty-two consecutive HIV-2 infected persons (17 men, 15 women) attending two different hospitals in Lisbon in 1997 were enrolled prospectively in the study. All but 4 individuals most likely acquired the infection through heterosexual contact. More than half of the study population was of African origin, mainly from Guinea-Bissau. Eleven (34.4%) patients had developed clinical manifestations included within the B or C groups of the CDC classification system for HIV infection, with the rest being asymptomatic. Half of the population was undergoing antiretroviral treatment at the time of the study. HIV-2 subtypes were investigated using a new Nef-based restriction fragment length polymorphism (RFLP) method that allows differentiation of the main two variants, A and B. Plasma viral load was quantified using a new quantitative competitive reverse transcriptase polymerase chain reaction (QcRT-PCR) procedure as well as the Amp-RT assay. Virus isolation was attempted from peripheral blood mononuclear cells. All but one person carried HIV-2 subtype A. Plasma viraemia examined by QcRT-PCR was measurable in 15 (50%) of 30 subjects, yielding in all instances values below 20,000 HIV-2 RNA copies per ml. Plasma RT activity could be detected in only 10 (33%) of 30 subjects, a rate much lower than that seen in HIV-1 infection. Virus was isolated from 16 (53.3%) of 30 patients. A significant correlation was found between CD4+ counts, clinical status, rate of virus isolation, and plasma viral load by both QcRT-PCR and Amp-RT. In conclusion, HIV-2 subtype A is the predominant variant circulating in Portugal among both natives and immigrants. A lower cellular and plasma viral load with respect to HIV-1 was seen in persons without immunosuppression, from whom the rate of virus recovery was extremely low.

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Section: Discussionmentioning

confidence: 73%

Section: Introductionmentioning

confidence: 99%

Human immunodeficiency virus type 2 (HIV-2) in Portugal: Clinical spectrum, circulating subtypes, virus isolation, and plasma viral load

et al. 2000

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“…Until recently, recombinations in vivo between HIV or SIV were rarely described, because for recombination to occur, individuals must be coinfected with divergent strains and because most naturally occurring recombination events would generate nonfunctional viruses, or at least viruses with reduced fitness, which are harder to identify. However, an increasing number of reports based on phylogenetic analysis have strongly suggested that recombination occurs in HIV-infected individuals (6,8,13,40,46,48,53,66). SIVmac recombination in macaques has been directly demonstrated by Wooley et al, by the simultaneous inoculation of a naive monkey with two SIVmac239 viruses, attenuated by different deletions (69).…”

Section: Vol 75 2001mentioning

confidence: 99%

Persistence of Pathogenic Challenge Virus in Macaques Protected by Simian Immunodeficiency Virus SIVmacΔ nef

Khatissian

Monceaux

Cumont

et al. 2001

J Virol

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Live attenuated simian immunodeficiency virus (SIV) is the most efficient vaccine yet developed in monkey models of human immunodeficiency virus infection. In all successful vaccine trials, attenuation was achieved by inactivating at least the nef gene. We investigated some virological and immunological characteristics of five rhesus macaques immunized with a nef-inactivated SIVmac251 molecular clone (SIVmac251⌬nef) and challenged 15 months later with the pathogenic SIVmac251 isolate. Three animals were killed 2 weeks postchallenge (p.c.) to search for the challenge virus and to assess immunological changes in various organs. The other two animals have been monitored up for 7 years p.c., with clinical and nef gene changes being noted. The animals killed showed no increase in viral load and no sign of a secondary immune response, although the challenged virus was occasionally detected by PCR. In one of the monkeys being monitored, the vaccine virus persisted and an additional deletion occured in nef. In the other monkey that was monitored, the challenge and the vaccine (⌬nef) viruses were both detected by PCR until a virus with a hybrid nef allele was isolated 48 months p.c. This nef hybrid encodes a 245-amino-acid protein. Thus, our results show (i) that monkeys were not totally protected against homologous virus challenge but controlled the challenge very efficiently in the absence of a secondary immune response, and (ii) that the challenge and vaccine viruses may persist in a replication-competent form for long periods after the challenge, possibly resulting in recombination between the two viruses.

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“…In the Marseilles area, HIV-2 is responsible for approximately 0.6% of cases of HIV infections and 0.4% of cases of AIDS. Seven HIV-2 subtypes, A through G, have been identified to date (8,17,27,38,46), but subtype A is the most common worldwide (17,46) and in France (11). Although both HIV-1 and HIV-2 can cause AIDS and have similar clinical and biological characteristics (9,19), major differences can be highlighted: plasma HIV RNA titers are lower in HIV-2-infected patients than in HIV-1-infected patients (3,4,12,30,35), individuals infected with HIV-2 have a slower disease progression (2,24,37,44), and HIV-2 shows lower transmissibility (1,2,23,24,44) compared with HIV-1.…”

mentioning

confidence: 99%

Polymorphism and Drug-Selected Mutations in the Protease Gene of Human Immunodeficiency Virus Type 2 from Patients Living in Southern France

et al. 2004

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The susceptibility of human immunodeficiency virus type 2 (HIV-2) to protease inhibitors (PI) is largely unknown. We studied HIV-2 protease genes from 21 HIV-2-infected patients who were exposed or not exposed to PI. The aim of this study was (i) to characterize the polymorphism of HIV-2 protease in the absence of drug, (ii) to know whether the HIV-2 protease gene naturally harbors HIV-1 drug resistance codons, and (iii) to identify mutations emerging under PI-selective pressure. Sixty-five HIV-2 RNA or proviral DNA samples were directly sequenced from the plasma or peripheral blood mononuclear cells of 8 patients who had received PI and 13 patients who had never received any antiretroviral. In untreated patients, the highest amino acid variability in HIV-2 protease was observed at positions 14, 40, 43, 46, 65 and 70, and seven codons (10V, 32I, 36I, 46I, 47V, 71V, and 73A) associated with drug resistance in HIV-1 were highly prevalent. In addition, at six positions (positions 7, 46, 62, 71, 90, and 99), the amino acid variability or the amino acid frequencies or both differed significantly in PI-treated and untreated patients, suggesting that mutations 7K3R, 46V3I, 62V3A/T, 71V3I, 90L3M and 99L3F were occurring under PI-selective pressure. At these positions, at least one sample simultaneously harbored both wild-type and mutated codons, while substitutions at positions 62, 71, 90, and 99 were confirmed in a longitudinal analysis. Moreover, the presence of codons 46I and 99F in the absence of drug in HIV-2 subtype B proteases may reflect natural resistance to PI. In conclusion, the present study revealed that HIV-2 strains harbor specific patterns of natural polymorphism and resistance.

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Phylogenetic Analysis of HIV Type 2 in Ghana and Intrasubtype Recombination in HIV Type 2

Cited by 18 publications

References 12 publications

Human immunodeficiency virus type 2 (HIV-2) in Portugal: Clinical spectrum, circulating subtypes, virus isolation, and plasma viral load

Human immunodeficiency virus type 2 (HIV-2) in Portugal: Clinical spectrum, circulating subtypes, virus isolation, and plasma viral load

Persistence of Pathogenic Challenge Virus in Macaques Protected by Simian Immunodeficiency Virus SIVmacΔ nef

Polymorphism and Drug-Selected Mutations in the Protease Gene of Human Immunodeficiency Virus Type 2 from Patients Living in Southern France

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