Infection of the CD45RA+ (Naive) Subset of Peripheral CD8+ Lymphocytes by Human Immunodeficiency Virus Type 1 In Vivo

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Published inJournal of Virology Vol. 75; no. 9; pp. 4091 - 4102
Main Authors McBreen, S., Imlach, S., Shirafuji, T., Scott, G. R., Leen, C., Bell, J. E., Simmonds, P.
Format Journal Article
LanguageEnglish
Published United States American Society for Microbiology 01.05.2001
Subjects
Amino Acid Sequence
Base Sequence
CD4-Positive T-Lymphocytes - virology
CD8-Positive T-Lymphocytes - immunology
CD8-Positive T-Lymphocytes - virology
DNA, Viral
HIV Infections - blood
HIV Infections - drug therapy
HIV Infections - immunology
HIV Infections - virology
HIV Long Terminal Repeat
HIV-1 - classification
HIV-1 - genetics
HIV-1 - immunology
HIV-1 - physiology
Humans
Immunologic Memory
Leukocyte Common Antigens - immunology
Molecular Sequence Data
Pathogenesis and Immunity
Protein Tyrosine Phosphatase, Non-Receptor Type 1
Proviruses - classification
Proviruses - genetics
Proviruses - immunology
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Abstract Article Usage Stats Services JVI Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley Reddit StumbleUpon Twitter current issue Spotlights in the Current Issue JVI About JVI Subscribers Authors Reviewers Advertisers Inquiries from the Press Permissions & Commercial Reprints ASM Journals Public Access Policy JVI RSS Feeds 1752 N Street N.W. • Washington DC 20036 202.737.3600 • 202.942.9355 fax • journals@asmusa.org Print ISSN: 0022-538X Online ISSN: 1098-5514 Copyright © 2014 by the American Society for Microbiology.   For an alternate route to JVI .asm.org, visit: JVI       
AbstractList To investigate the mechanism and functional significance of infection of CD8 + lymphocytes by human immunodeficiency virus type 1 (HIV-1) in vivo, we determined frequencies of infection, proviral conformation, and genetic relationships between HIV-1 variants infecting naive (CD45RA + ) and memory (CD45RO + ) peripheral blood CD4 + and CD8 + lymphocytes. Infection of CD3 + CD8 + CD45RA + cells was detected in 9 of 16 study subjects at frequencies ranging from 30 to 1,400 proviral copies/10 6 cells, more frequently than CD3 + CD8 + lymphocytes expressing the RO isoform of CD45 ( n = 2, 70 and 260 copies /10 6 cells). In agreement with previous studies, there was no evidence for a similar preferential infection of CD4 + naive lymphocytes. Proviral sequences in both CD4 + and CD8 + lymphocyte subsets were complete, as assessed by quantitation using primers from the long terminal repeat region spanning the tRNA primer binding site. In six of the seven study subjects investigated, variants infecting CD8 + lymphocytes were partially or completely genetically distinct in the V3 region from those recovered from CD4 + lymphocytes and showed a greater degree of compartmentalization than observed between naive and memory subsets of CD4 + lymphocytes. In two study subjects, arginine substitutions at position 306, associated with use of the chemokine coreceptor CXCR4, were preferentially found in CD4 lymphocytes. These population differences may have originated through different times of infection rather than necessarily indicating a difference in their biological properties. The preferential distribution of HIV-1 in naive CD8 + lymphocytes indeed suggests that infection occurred early in T-lymphocyte ontogeny, such as during maturation in the thymus. Destruction of cells destined to become CD8 + lymphocytes may be a major factor in the decline in CD8 + lymphocyte frequencies and function on disease progression and may contribute directly to the observed immunodeficiency in AIDS.
To investigate the mechanism and functional significance of infection of CD8+ lymphocytes by human immunodeficiency virus type 1 (HIV-1) in vivo, we determined frequencies of infection, proviral conformation, and genetic relationships between HIV-1 variants infecting naive (CD45RA+) and memory (CD45RO+) peripheral blood CD4+ and CD8+ lymphocytes. Infection of CD3+ CD8+ CD45RA+ cells was detected in 9 of 16 study subjects at frequencies ranging from 30 to 1,400 proviral copies/10(6) cells, more frequently than CD3+ CD8+ lymphocytes expressing the RO isoform of CD45 (n = 2, 70 and 260 copies /10(6) cells). In agreement with previous studies, there was no evidence for a similar preferential infection of CD4+ naive lymphocytes. Proviral sequences in both CD4+ and CD8+ lymphocyte subsets were complete, as assessed by quantitation using primers from the long terminal repeat region spanning the tRNA primer binding site. In six of the seven study subjects investigated, variants infecting CD8+ lymphocytes were partially or completely genetically distinct in the V3 region from those recovered from CD4+ lymphocytes and showed a greater degree of compartmentalization than observed between naive and memory subsets of CD4+ lymphocytes. In two study subjects, arginine substitutions at position 306, associated with use of the chemokine coreceptor CXCR4, were preferentially found in CD4 lymphocytes. These population differences may have originated through different times of infection rather than necessarily indicating a difference in their biological properties. The preferential distribution of HIV-1 in naive CD8+ lymphocytes indeed suggests that infection occurred early in T-lymphocyte ontogeny, such as during maturation in the thymus. Destruction of cells destined to become CD8+ lymphocytes may be a major factor in the decline in CD8+ lymphocyte frequencies and function on disease progression and may contribute directly to the observed immunodeficiency in AIDS.To investigate the mechanism and functional significance of infection of CD8+ lymphocytes by human immunodeficiency virus type 1 (HIV-1) in vivo, we determined frequencies of infection, proviral conformation, and genetic relationships between HIV-1 variants infecting naive (CD45RA+) and memory (CD45RO+) peripheral blood CD4+ and CD8+ lymphocytes. Infection of CD3+ CD8+ CD45RA+ cells was detected in 9 of 16 study subjects at frequencies ranging from 30 to 1,400 proviral copies/10(6) cells, more frequently than CD3+ CD8+ lymphocytes expressing the RO isoform of CD45 (n = 2, 70 and 260 copies /10(6) cells). In agreement with previous studies, there was no evidence for a similar preferential infection of CD4+ naive lymphocytes. Proviral sequences in both CD4+ and CD8+ lymphocyte subsets were complete, as assessed by quantitation using primers from the long terminal repeat region spanning the tRNA primer binding site. In six of the seven study subjects investigated, variants infecting CD8+ lymphocytes were partially or completely genetically distinct in the V3 region from those recovered from CD4+ lymphocytes and showed a greater degree of compartmentalization than observed between naive and memory subsets of CD4+ lymphocytes. In two study subjects, arginine substitutions at position 306, associated with use of the chemokine coreceptor CXCR4, were preferentially found in CD4 lymphocytes. These population differences may have originated through different times of infection rather than necessarily indicating a difference in their biological properties. The preferential distribution of HIV-1 in naive CD8+ lymphocytes indeed suggests that infection occurred early in T-lymphocyte ontogeny, such as during maturation in the thymus. Destruction of cells destined to become CD8+ lymphocytes may be a major factor in the decline in CD8+ lymphocyte frequencies and function on disease progression and may contribute directly to the observed immunodeficiency in AIDS.
Article Usage Stats Services JVI Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley Reddit StumbleUpon Twitter current issue Spotlights in the Current Issue JVI About JVI Subscribers Authors Reviewers Advertisers Inquiries from the Press Permissions & Commercial Reprints ASM Journals Public Access Policy JVI RSS Feeds 1752 N Street N.W. • Washington DC 20036 202.737.3600 • 202.942.9355 fax • journals@asmusa.org Print ISSN: 0022-538X Online ISSN: 1098-5514 Copyright © 2014 by the American Society for Microbiology.   For an alternate route to JVI .asm.org, visit: JVI       
To investigate the mechanism and functional significance of infection of CD8+ lymphocytes by human immunodeficiency virus type 1 (HIV-1) in vivo, we determined frequencies of infection, proviral conformation, and genetic relationships between HIV-1 variants infecting naive (CD45RA+) and memory (CD45RO+) peripheral blood CD4+ and CD8+ lymphocytes. Infection of CD3+ CD8+ CD45RA+ cells was detected in 9 of 16 study subjects at frequencies ranging from 30 to 1,400 proviral copies/10(6) cells, more frequently than CD3+ CD8+ lymphocytes expressing the RO isoform of CD45 (n = 2, 70 and 260 copies /10(6) cells). In agreement with previous studies, there was no evidence for a similar preferential infection of CD4+ naive lymphocytes. Proviral sequences in both CD4+ and CD8+ lymphocyte subsets were complete, as assessed by quantitation using primers from the long terminal repeat region spanning the tRNA primer binding site. In six of the seven study subjects investigated, variants infecting CD8+ lymphocytes were partially or completely genetically distinct in the V3 region from those recovered from CD4+ lymphocytes and showed a greater degree of compartmentalization than observed between naive and memory subsets of CD4+ lymphocytes. In two study subjects, arginine substitutions at position 306, associated with use of the chemokine coreceptor CXCR4, were preferentially found in CD4 lymphocytes. These population differences may have originated through different times of infection rather than necessarily indicating a difference in their biological properties. The preferential distribution of HIV-1 in naive CD8+ lymphocytes indeed suggests that infection occurred early in T-lymphocyte ontogeny, such as during maturation in the thymus. Destruction of cells destined to become CD8+ lymphocytes may be a major factor in the decline in CD8+ lymphocyte frequencies and function on disease progression and may contribute directly to the observed immunodeficiency in AIDS.
Author C. Leen
S. Imlach
T. Shirafuji
J. E. Bell
P. Simmonds
S. McBreen
G. R. Scott
AuthorAffiliation Laboratory for Clinical and Molecular Virology, University of Edinburgh, Edinburgh EH9 1QH, 1 Department of Genitourinary Medicine, Royal Infirmary of Edinburgh, Edinburgh EH3 9YW, 2 and Regional Infectious Diseases Unit 3 and Department of Neuropathology, 4 Western General Hospital, Edinburgh EH4 2XU, United Kingdom
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/11287558$$D View this record in MEDLINE/PubMed
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Corresponding author. Mailing address: Laboratory for Clinical and Molecular Virology, University of Edinburgh, Summerhall, Edinburgh EH9 1QH, United Kingdom. Phone: 44 131 650 7927. Fax: 44 131 650 7965. E-mail: Peter.Simmonds@ed.ac.uk.
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To investigate the mechanism and functional significance of infection of CD8 + lymphocytes by human immunodeficiency virus type 1 (HIV-1) in vivo, we...
To investigate the mechanism and functional significance of infection of CD8+ lymphocytes by human immunodeficiency virus type 1 (HIV-1) in vivo, we determined...
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SubjectTerms Amino Acid Sequence
Base Sequence
CD4-Positive T-Lymphocytes - virology
CD8-Positive T-Lymphocytes - immunology
CD8-Positive T-Lymphocytes - virology
DNA, Viral
HIV Infections - blood
HIV Infections - drug therapy
HIV Infections - immunology
HIV Infections - virology
HIV Long Terminal Repeat
HIV-1 - classification
HIV-1 - genetics
HIV-1 - immunology
HIV-1 - physiology
Humans
Immunologic Memory
Leukocyte Common Antigens - immunology
Molecular Sequence Data
Pathogenesis and Immunity
Protein Tyrosine Phosphatase, Non-Receptor Type 1
Proviruses - classification
Proviruses - genetics
Proviruses - immunology
Title Infection of the CD45RA+ (Naive) Subset of Peripheral CD8+ Lymphocytes by Human Immunodeficiency Virus Type 1 In Vivo
URI http://jvi.asm.org/content/75/9/4091.abstract
https://www.ncbi.nlm.nih.gov/pubmed/11287558
https://www.proquest.com/docview/77031133
https://pubmed.ncbi.nlm.nih.gov/PMC114154
Volume 75
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