HIV-1 subtype O: epidemiology, pathogenesis, diagnosis, and perspectives of the evolution of HIV

Gürtler, Lutz; Zekeng, Léopold; Tsague, J.M.; Brunn, Albrecht von; Ze, E. Afane; Eberle, Josef; Kaptué, Lazare

doi:10.1007/978-3-7091-7482-1_17

Cited by 16 publications

(13 citation statements)

References 13 publications

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“…Blood (8 mL) was drawn into Vacutainer CP tubes and processed according to the manufacturer's instructions (Becton Dickinson, Franklin Lakes, NJ). Total cellular DNA was prepared by lysis of 6 4 ϫ 10 peripheral blood lymphocytes/mL in lysis buffer (10 mM Tris [pH 8.3]/0.05% Triton X-100), addition of 10 mg/mL proteinase K, incubation at 56ЊC for 1 h, and inactivation of proteinase K at 95ЊC for 10 min. env gp41 [11], env C2V3 [11], gag p17 [11], and core p24 [12] PCR amplification conditions and primer sequences were as described elsewhere.…”

Section: Methodsmentioning

confidence: 99%

“…The highest prevalence of HIV-1 group O infections is in the Central African country of Cameroon [6,7], which is also the country of origin for the first reported case of group N HIV [2]. Serosurveillance in the United States of 1057 serum samples from high-and low-risk persons did not reveal any sample with serologic evidence of group O HIV-1 infection [8].…”

mentioning

confidence: 94%

“…Most group O HIV-1 infections have been identified in Africa; much smaller numbers of infections have been identified in Europe [6]. The highest prevalence of HIV-1 group O infections is in the Central African country of Cameroon [6,7], which is also the country of origin for the first reported case of group N HIV [2].…”

mentioning

confidence: 98%

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Human Immunodeficiency Virus (HIV) Subtype Surveillance of African‐Born Persons at Risk for Group O and Group N HIV Infections in the United States

Sullivan

Ellenberger

et al. 2000

J INFECT DIS

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A population-based surveillance registry was used to identify human immunodeficiency virus (HIV)-infected persons in the United States at increased risk for group O and group N infections (those born in or near African countries where group O infection has been reported). Of 155 eligible subjects, 37 gave samples. By phylogenetic and serologic analysis, 32 were infected with group M (16 with subtype A, 5 with B, 7 with C, and 1 each with subtypes D, F2, G, and recombinant A/J) and 2 with group O but none with group N virus. For 3, samples could not be typed by serology or amplified by polymerase chain reaction using group M-, O-, or N-specific primers. In the United States, group O HIV infection is uncommon; no case of group N infection was found. African-born persons may have HIV strains typical of their birth country. Ongoing subtype surveillance may allow early identification of novel or emerging HIV strains.

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Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 94%

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Human Immunodeficiency Virus (HIV) Subtype Surveillance of African‐Born Persons at Risk for Group O and Group N HIV Infections in the United States

Sullivan

Ellenberger

et al. 2000

J INFECT DIS

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“…Cell-free supernatants were assayed for reverse transcriptase (RT) activity by [␣-32 P]dTTP incorporation, as described previously (34), and [␣-32 P]dTTP incorporation was quantitated using an Instant (15). Viral titers were determined by infecting MAGI indicator cell lines as described previously (19).…”

mentioning

confidence: 99%

An Exonic Splicing Silencer Downstream of the 3′ Splice Site A2 Is Required for Efficient Human Immunodeficiency Virus Type 1 Replication

Madsen¹,

Stoltzfus

2005

J Virol

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Alternative splicing of the human immunodeficiency virus type 1 (HIV-1) genomic mRNA produces more than 40 unique viral mRNA species, of which more than half remain incompletely spliced within an HIV-1-infected cell. Regulation of splicing at HIV-1 3 splice sites (3ss) requires suboptimal polypyrimidine tracts, and positive or negative regulation of splicing occurs through binding of cellular factors to cis-acting splicing regulatory elements. We have previously shown that splicing at HIV-1 3ss A2, which produces vpr mRNA and promotes inclusion of HIV-1 exon 3, is repressed by the hnRNP A/B-dependent exonic splicing silencer ESSV. Here we show that ESSV activity downstream of 3ss A2 is localized to a 16-nucleotide element within HIV-1 exon 3. HIV-1 replication was reduced by 95% when ESSV was inactivated by mutagenesis. Reduced replication was concomitant with increased inclusion of exon 3 within spliced viral mRNA and decreased accumulation of unspliced viral mRNA, resulting in decreased cell-associated p55 Gag. Prolonged culture of ESSV mutant viruses resulted in two independent second-site reversions disrupting the splice sites that define exon 3, 3ss A2 and 5 splice site D3. Either of these changes restored both HIV-1 replication and regulated viral splicing. Therefore, inhibition of HIV-1 3ss A2 splicing is necessary for HIV-1 replication.In contrast to the alternative splicing of most cellular mRNA, splicing of retroviral mRNA results in the cytoplasmic accumulation of incompletely spliced and unspliced viral mRNA. Incompletely spliced viral mRNA is necessary for the expression of the Env, Vpu, Vpr, and Vif proteins, and the accumulation of unspliced viral mRNA is necessary for expression of the gag and pol gene products and also serves as the genomic viral mRNA encapsidated within progeny virions. Completely spliced viral mRNA is required for expression of the regulatory viral proteins Tat, Rev, and Nef. More than 40 unique incompletely and completely spliced viral mRNA species are generated through the alternative splicing of the HIV-1 primary transcript within an HIV-1-infected cell (23,26).HIV-1 3Ј splice sites (3Јss) are used with differing efficiencies in part because viral polypyrimidine tracts (PPT) are interspersed with purines (27, 30), leading to decreased affinity for the essential cellular splicing factor U2AF65 (for a review of cellular splicing see reference 12). In addition, the efficiency of HIV-1 splicing is also regulated by both positive and negative cis elements within the viral genome that act to promote or repress splicing. To date, four exonic splicing silencers (ESS) and one intronic splicing silencer (ISS) have been identified within the viral genome (Fig. 1). Utilization of HIV-1 3Јss A2 by the spliceosome is negatively regulated by ESSV, 3Јss A3 by ESSp and ESS2, and 3Јss A7 by the ISS and ESS3 (2,3,5,16,29,31).We have previously characterized ESSV as a 24-nucleotide

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“…Entsprechend der phylogenetischen Entwicklung der Affen kommt daher für die Evolution von SIV ein Zeitraum von mehreren hunderttausend bzw. Millionen Jahren in Betracht [37].…”

Section: Sivsm Als Quelle Für Hiv-2unclassified

SIV als Quelle von HIV

Gürtler

2004

Bundesgesundheitsbl - Gesundheitsforsch - Gesundheitsschutz

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It is assumed that HIV, the human immunodeficiency virus, started its spread after the Second World War. Molecular analysis of the genome of various HIV-1 types has shown that this virus can be divided into the groups M, N, and O and that these genome sequences fit perfectly to the genomes found in SIV of chimpanzees (SIVcpz) living in the area of West and Central Africa. SIVcpz is nonpathogenic for chimpanzees indicating that the virus and host have adapted for a long period. HIV-2 genome sequences converge with SIV sequences of sooty mangabey monkeys from West Africa (SIVsm), covering the subtypes A to G from HIV-2. SIVsm is nonpathogenic for mangabey monkeys. All available data indicate that HIV-1 and HIV-2 have been introduced into humans at least several times. Since SIVcpz and SIVs from other monkeys are recombinant viruses, it cannot be excluded that a new recombinant SIV might again enter the human population and initiate a new epidemic.

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HIV-1 subtype O: epidemiology, pathogenesis, diagnosis, and perspectives of the evolution of HIV

Cited by 16 publications

References 13 publications

Human Immunodeficiency Virus (HIV) Subtype Surveillance of African‐Born Persons at Risk for Group O and Group N HIV Infections in the United States

Human Immunodeficiency Virus (HIV) Subtype Surveillance of African‐Born Persons at Risk for Group O and Group N HIV Infections in the United States

An Exonic Splicing Silencer Downstream of the 3′ Splice Site A2 Is Required for Efficient Human Immunodeficiency Virus Type 1 Replication

SIV als Quelle von HIV

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