scholarly journals Association of Polymorphisms in Human Leukocyte Antigen Class I and Transporter Associated with Antigen Processing Genes with Resistance to Human Immunodeficiency Virus Type 1 Infection

2003 ◽  
Vol 187 (9) ◽  
pp. 1404-1410 ◽  
Author(s):  
Chenglong Liu ◽  
Mary Carrington ◽  
Richard A. Kaslow ◽  
Xiaojiang Gao ◽  
Charles R. Rinaldo ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Human Leukocyte Antigen ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
Antigen Processing ◽  
Human Leukocyte Antigen Class ◽  
Human Leukocyte ◽  
Leukocyte Antigen ◽  
Immunodeficiency Virus

scholarly journals Human Leukocyte Antigen B58 Supertype and Human Immunodeficiency Virus Type 1 Infection in Native Africans

2006 ◽  
Vol 80 (12) ◽  
pp. 6056-6060 ◽  
Author(s):  
Aleksandr Lazaryan ◽  
Elena Lobashevsky ◽  
Joseph Mulenga ◽  
Etienne Karita ◽  
Susan Allen ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Human Leukocyte Antigen ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
Human Leukocyte ◽  
Subtype C ◽  
Leukocyte Antigen ◽  
Immunodeficiency Virus ◽  
Hiv 1

ABSTRACT Human leukocyte antigen (HLA) class I alleles can be grouped into supertypes according to their shared peptide binding properties. We examined alleles of the HLA-B58 supertype (B58s) in treatment-naïve human immunodeficiency virus type 1 (HIV-1)-seropositive Africans (423 Zambians and 202 Rwandans). HLA-B and HLA-C alleles were resolved to four digits by a combination of molecular methods, and their respective associations with outcomes of HIV-1 infection were analyzed by statistical procedures appropriate for continuous or categorical data. The effects of the individual alleles on natural HIV-1 infection were heterogeneous. In HIV-1 subtype C-infected Zambians, the mean viral load (VL) was lower among B*5703 (P = 0.01) or B*5703-Cw*18 (P < 0.001) haplotype carriers and higher among B*5802 (P = 0.02) or B*5802-Cw*0602 (P = 0.03) carriers. The B*5801-Cw*03 haplotype showed an association with low VL (P = 0.05), whereas B*5801 as a whole did not. Rwandans with HIV-1 subtype A infection showed associations of B*5703 and B*5802 with slow (P = 0.06) and rapid (P = 0.003) disease progression, respectively. In neither population were B*1516-B*1517 alleles associated with more favorable responses. Overall, B58s alleles, individually or as part of an HLA-B-HLA-C haplotype, appeared to have a distinctive impact on HIV-1 infection among native Africans. As presently defined, B58s alleles cannot be considered uniformly protective against HIV/AIDS in every population.

scholarly journals Discordance at Human Leukocyte Antigen–DRB3 and Protection from Human Immunodeficiency Virus Type 1 Transmission

2002 ◽  
Vol 185 (12) ◽  
pp. 1729-1735 ◽  
Author(s):  
Shannon L. Hader ◽  
Thomas W. Hodge ◽  
Kate A. Buchacz ◽  
Robert A. Bray ◽  
Nancy S. Padian ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Human Leukocyte Antigen ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
Human Leukocyte ◽  
Leukocyte Antigen ◽  
Immunodeficiency Virus

scholarly journals Proline 78 Is Crucial for Human Immunodeficiency Virus Type 1 Nef To Down-Regulate Class I Human Leukocyte Antigen

2003 ◽  
Vol 77 (2) ◽  
pp. 1589-1594 ◽  
Author(s):  
Takeshi Yamada ◽  
Naotoshi Kaji ◽  
Takashi Odawara ◽  
Joe Chiba ◽  
Aikichi Iwamoto ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
T Lymphocytes ◽  
Human Leukocyte Antigen ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
Human Leukocyte ◽  
Down Regulation ◽  
Leukocyte Antigen ◽  
Immunodeficiency Virus

ABSTRACT Human immunodeficiency virus type 1 Nef down-regulates human leukocyte antigen class I (HLA-I) in T lymphocytes, and the down-regulation involves the Nef proline-rich domain (PRD) containing four prolines at positions 69, 72, 75, and 78. We used a Sendai virus vector with nef and examined regulation by Nef of HLA-I and CD4 in suspension cultures of cells such as T lymphocytes. Analyses of a series of PRD substitution mutants indicated that, because the substitution of Pro78 with Ala abolished down-regulation of HLA-I but not of CD4, Pro78 is important for HLA-I down-regulation in T lymphocytes.

scholarly journals Human Immunodeficiency Virus Type 1 Evades T-Helper Responses by Exploiting Antibodies That Suppress Antigen Processing

2004 ◽  
Vol 78 (14) ◽  
pp. 7645-7652 ◽  
Author(s):  
Peter C. Chien ◽  
Sandra Cohen ◽  
Michael Tuen ◽  
James Arthos ◽  
Pei-de Chen ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
T Cells ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
Antigen Processing ◽  
T Helper ◽  
Peptide Epitopes ◽  
Immunodeficiency Virus ◽  
Hiv 1

ABSTRACT T-helper responses are important for controlling chronic viral infections, yet T-helper responses specific to human immunodeficiency virus type 1 (HIV-1), particularly to envelope glycoproteins, are lacking in the vast majority of HIV-infected individuals. It was previously shown that the presence of antibodies to the CD4-binding domain (CD4bd) of HIV-1 glycoprotein 120 (gp120) prevents T-helper responses to gp120, but their suppressive mechanisms were undefined (C. E. Hioe et al., J. Virol. 75:10950-10957, 2001). The present study demonstrates that gp120, when complexed to anti-CD4bd antibodies, becomes more resistant to proteolysis by lysosomal enzymes from antigen-presenting cells such that peptide epitopes are not released and presented efficiently by major histocompatibility complex class II molecules to gp120-specific CD4 T cells. Antibodies to other gp120 regions do not confer this effect. Thus, HIV may evade anti-viral T-helper responses by inducing and exploiting antibodies that conceal the virus envelope antigens from T cells.

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