HIV-2 capsids distinguish high and low virus load patients in a West African community cohort

HIV-2 causes AIDS similar to HIV-1, however a considerable proportion of HIV-2 infected patients show no disease and have low plasma virus load (VL). An analysis of HIV-2 capsid (p26) variation demonstrated that proline at p26 positions 119, 159 and 178 are more frequent in lower VL subjects while n...

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Published inVaccine Vol. 28; no. S2; pp. B60 - B67
Main Authors Onyango, Clayton O., Leligdowicz, Aleksandra, Yokoyama, Masaru, Sato, Hironori, Song, Haihan, Nakayama, Emi E., Shioda, Tatsuo, de Silva, Thushan, Townend, John, Jaye, Assan, Whittle, Hilton, Rowland-Jones, Sarah, Cotten, Matthew
Format Journal Article
LanguageEnglish
Published Netherlands Elsevier Ltd 26.05.2010
Elsevier Limited
Subjects
Acquired immune deficiency syndrome
AIDS
Allergy and Immunology
Antiviral Restriction Factors
Capsid
Capsid - virology
Carrier Proteins - metabolism
Cohort Studies
Deoxyribonucleic acid
DNA
gag Gene Products, Human Immunodeficiency Virus - metabolism
Guinea-Bissau
HIV
HIV Infections - virology
HIV-2
HIV-2 - genetics
HIV-2 - pathogenicity
HIV-2 - physiology
Human immunodeficiency virus
Human immunodeficiency virus 1
Human immunodeficiency virus 2
Humans
Infections
Models, Molecular
Patients
Phylogenetics
Phylogeny
Plasma
Polymerase chain reaction
Polymorphism, Genetic
RNA, Viral - genetics
Sequence Analysis, Protein
Studies
TRIM5α
Tripartite Motif Proteins
Ubiquitin-Protein Ligases
Viral Load
Virus Replication
Viruses
Guinea-Bissau
Guinea Bissau
Capsid
TRIM5α
HIV-2
Online AccessGet full text
ISSN0264-410X
1873-2518
1873-2518
DOI10.1016/j.vaccine.2009.08.060

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Abstract HIV-2 causes AIDS similar to HIV-1, however a considerable proportion of HIV-2 infected patients show no disease and have low plasma virus load (VL). An analysis of HIV-2 capsid (p26) variation demonstrated that proline at p26 positions 119, 159 and 178 are more frequent in lower VL subjects while non-proline residues at all three sites are more frequent in subjects with high VL. In vitro replication levels of viruses bearing changes at the three sites suggested that these three residues influence virus replication by altering susceptibility to TRIM5α. These results provide new insights into HIV-2 pathogenesis.
AbstractList HIV-2 causes AIDS similar to HIV-1, however a considerable proportion of HIV-2 infected patients show no disease and have low plasma virus load (VL). An analysis of HIV-2 capsid (p26) variation demonstrated that proline at p26 positions 119, 159 and 178 are more frequent in lower VL subjects while non-proline residues at all three sites are more frequent in subjects with high VL. In vitro replication levels of viruses bearing changes at the three sites suggested that these three residues influence virus replication by altering susceptibility to TRIM5α. These results provide new insights into HIV-2 pathogenesis.
Abstract HIV-2 causes AIDS similar to HIV-1, however a considerable proportion of HIV-2 infected patients show no disease and have low plasma virus load (VL). An analysis of HIV-2 capsid (p26) variation demonstrated that proline at p26 positions 119, 159 and 178 are more frequent in lower VL subjects while non-proline residues at all three sites are more frequent in subjects with high VL. In vitro replication levels of viruses bearing changes at the three sites suggested that these three residues influence virus replication by altering susceptibility to TRIM5α. These results provide new insights into HIV-2 pathogenesis.
HIV-2 causes AIDS similar to HIV-1, however a considerable proportion of HIV-2 infected patients show no disease and have low plasma virus load (VL). An analysis of HIV-2 capsid (p26) variation demonstrated that proline at p26 positions 119, 159 and 178 are more frequent in lower VL subjects while non-proline residues at all three sites are more frequent in subjects with high VL.In vitroreplication levels of viruses bearing changes at the three sites suggested that these three residues influence virus replication by altering susceptibility to TRIM5α. These results provide new insights into HIV-2 pathogenesis.
HIV-2 causes AIDS similar to HIV-1, however a considerable proportion of HIV-2 infected patients show no disease and have low plasma virus load (VL). An analysis of HIV-2 capsid (p26) variation demonstrated that proline at p26 positions 119, 159 and 178 are more frequent in lower VL subjects while non-proline residues at all three sites are more frequent in subjects with high VL. In vitro replication levels of viruses bearing changes at the three sites suggested that these three residues influence virus replication by altering susceptibility to TRIM5alpha. These results provide new insights into HIV-2 pathogenesis.
HIV-2 causes AIDS similar to HIV-1, however a considerable proportion of HIV-2 infected patients show no disease and have low plasma virus load (VL). An analysis of HIV-2 capsid (p26) variation demonstrated that proline at p26 positions 119, 159 and 178 are more frequent in lower VL subjects while non-proline residues at all three sites are more frequent in subjects with high VL. In vitro replication levels of viruses bearing changes at the three sites suggested that these three residues influence virus replication by altering susceptibility to TRIM5alpha. These results provide new insights into HIV-2 pathogenesis.HIV-2 causes AIDS similar to HIV-1, however a considerable proportion of HIV-2 infected patients show no disease and have low plasma virus load (VL). An analysis of HIV-2 capsid (p26) variation demonstrated that proline at p26 positions 119, 159 and 178 are more frequent in lower VL subjects while non-proline residues at all three sites are more frequent in subjects with high VL. In vitro replication levels of viruses bearing changes at the three sites suggested that these three residues influence virus replication by altering susceptibility to TRIM5alpha. These results provide new insights into HIV-2 pathogenesis.
HIV-2 causes AIDS similar to HIV-1, however a considerable proportion of HIV-2 infected patients show no disease and have low plasma virus load (VL). An analysis of HIV-2 capsid (p26) variation demonstrated that proline at p26 positions 119, 159 and 178 are more frequent in lower VL subjects while non-proline residues at all three sites are more frequent in subjects with high VL. replication levels of viruses bearing changes at the three sites suggested that these three residues influence virus replication by altering susceptibility to TRIM5 alpha . These results provide new insights into HIV-2 pathogenesis.
Author Jaye, Assan
Townend, John
Rowland-Jones, Sarah
Nakayama, Emi E.
Leligdowicz, Aleksandra
Sato, Hironori
Onyango, Clayton O.
de Silva, Thushan
Yokoyama, Masaru
Shioda, Tatsuo
Song, Haihan
Cotten, Matthew
Whittle, Hilton
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  email: mcotten@mrc.gm
  organization: Medical Research Council Laboratories, Fajara, Atlantic Road, P.O. Box 273, The Gambia
BackLink https://www.ncbi.nlm.nih.gov/pubmed/20510746$$D View this record in MEDLINE/PubMed
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HIV-2
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PublicationTitle Vaccine
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Snippet HIV-2 causes AIDS similar to HIV-1, however a considerable proportion of HIV-2 infected patients show no disease and have low plasma virus load (VL). An...
Abstract HIV-2 causes AIDS similar to HIV-1, however a considerable proportion of HIV-2 infected patients show no disease and have low plasma virus load (VL)....
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StartPage B60
SubjectTerms Acquired immune deficiency syndrome
AIDS
Allergy and Immunology
Antiviral Restriction Factors
Capsid
Capsid - virology
Carrier Proteins - metabolism
Cohort Studies
Deoxyribonucleic acid
DNA
gag Gene Products, Human Immunodeficiency Virus - metabolism
Guinea-Bissau
HIV
HIV Infections - virology
HIV-2
HIV-2 - genetics
HIV-2 - pathogenicity
HIV-2 - physiology
Human immunodeficiency virus
Human immunodeficiency virus 1
Human immunodeficiency virus 2
Humans
Infections
Models, Molecular
Patients
Phylogenetics
Phylogeny
Plasma
Polymerase chain reaction
Polymorphism, Genetic
RNA, Viral - genetics
Sequence Analysis, Protein
Studies
TRIM5α
Tripartite Motif Proteins
Ubiquitin-Protein Ligases
Viral Load
Virus Replication
Viruses
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Title HIV-2 capsids distinguish high and low virus load patients in a West African community cohort
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