HLA Class I and Plasma Viral Load of HIV-1 in Sexually Transmitted and Reproductive Tract Infections among Heterosexual Serodiscordant couples in Nigeria

ABSTRACTBackgroundThis study investigated HLA Class I in Long Term Non-progressors (LTNPs) and plasma viral load in Sexually Transmitted and Reproductive Tract Infections (STIs/RTIs) associated with Heterosexual HIV-1 transmission among serodiscordant couples in Nigeria.MethodsA total of 271 serodiscordant and concordant couples (HIV positive and negative) were enrolled, blood samples were collected from the subjects by venipuncture. HLA class I (with specific primers), plasma viral load, CD4+ analysis was done. Endocervical/urethral swabs and early morning urine samples were collected by standard microbiological methods. These were screened by microscopy, culture, antibiogram, and biochemical tests with a view to identify aetiologic agents of co-infections with HIV.ResultsThe Participants age ranged from ≥ 21- < 50years. The index whose plasma viral loads were 10,001-100,000 copies/ml had STIs/RTIs 32(60.9% p=0.059). Staphylococcus aureus and Escherichia coli (22.1%) were isolated from the index (HIV positive subject) while 14.5% of Staphylococcus aureus and 27.2% of E coli were isolated from their partners (HIV negative subject). Staphylococcus aureus and E coli are normal flora but because the patients are Immunocompromised as a result of positivity to HIV, Staphylococcus aureus and E. coli in this context becomes opportunistic thereby, causing genital tract infections. Staphylococcus from the index showed more sensitivity to Amoxicillin/clavulanate (95.4%/90.4%) compared to the partners (55.1%/73.5%) and more resistant to Ceftazidime (81.4%) compared to the partners (68.9%). LTNPs were 28(8.51%) among the index. HLA-B alleles: B*5701 (9.2%), B*5703 (4.6%) and B*5801(12.5%) were identified for viral control at late stage of HIV infection while A*1 (4.6%), and C*0701 (29.1%) were protective alleles observed. HLA-B*0702 (33.3%), B*4201/A*2301(4.6%) respectively were susceptible alleles associated with seroconversion among LTNPs.ConclusionThe microorganisms isolated from the index were associated with high viral loads and are independent makers to HIV-1 transmission among serodiscordant couples. Individuals associated with HLA class I alleles identified among LTNPs were those significantly associated with resistance and susceptible to HIV-1 infections.

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Characteristics allelic of Human Leukocyte Antigen class I genotype and association with viral load and CD4 cell count in HIV-1 infected patients, Hanoi 2014 – 2016

Tạp chí Y học Dự phòng ◽

10.51403/0868-2836/2021/335 ◽

2021 ◽

Vol 31 (4) ◽

pp. 43-50

Author(s):

Tran Thi Minh Tam ◽

Nguyen Thuy Linh ◽

Phan Ha My ◽

Nguyen Thi Lan Anh

Keyword(s):

Viral Load ◽

Human Leukocyte ◽

Hla Class I ◽

Class I ◽

Cd4 Cell Count ◽

Leukocyte Antigen ◽

Cell Counts ◽

Cd4 Cell Counts ◽

Cd4 Cell ◽

Hiv 1

Human Leukocyte Antigen (HLA) class I plays a regulatory role in cellular immune response to HIV-1 infection. The role of HLA alleles in HIV progression via viral load and CD4 cell count is well known. HLA class I is polymorphic and distributed differently by nation. This descriptive cross-sectional study was performed on 303 HIV-1 infected patients in 2014 - 2016, with aims to (i) characterize HLA class I genotype with 4-digit nomenclature and (ii) identify specifc alleles in correlate with CD4 cell counts and HIV viral load. 117 allele genotypes have been identifed, including 28 HLA-A alleles, 54 HLA-B alleles and 35 HLA-C alleles. The results showed that the most prevalent alleles in the population include A*11:01 (30.7%), B*15:02 (15.2%) and C*08:01 (17.1%). The frequency of haplotype created from these alleles is 8.4%. A*02:03, B*46:01 related to gender and ethnicity respectively. In conclusion, the study provided detailed pattern of HLA class I expression in a study population of HIV-1 infected patients and reported for the frst time the associated B*51:01, C*14:02 alleles associated to an increase in CD4 cell counts.

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HLA-B*44 Is Associated with a Lower Viral Set Point and Slow CD4 Decline in a Cohort of Chinese Homosexual Men Acutely Infected with HIV-1

Clinical and Vaccine Immunology ◽

10.1128/cvi.00015-13 ◽

2013 ◽

Vol 20 (7) ◽

pp. 1048-1054 ◽

Cited By ~ 7

Author(s):

Xin Zhang ◽

XiaoJie Huang ◽

Wei Xia ◽

WeiHua Li ◽

Tong Zhang ◽

...

Keyword(s):

Viral Load ◽

T Cell ◽

T Cell Responses ◽

Hla Class I ◽

T Cell Response ◽

Class I ◽

Set Point ◽

Cell Responses ◽

Lower Magnitude ◽

Hiv 1

ABSTRACTHLA class I alleles have been shown to have differential impacts on the viral load and the outcome of HIV-1 disease progression. In this study, HLA class I types from residents of China with acute HIV-1 infection, diagnosed between 2006 and 2011, were identified and the association between expression of individual HLA alleles and the level of the set point viral load was analyzed. A lower level of set point viral load was found to be associated with the Bw4 homozygote on HLA-B alleles. B*44 and B*57 alleles have also been found to be associated with lower set point viral load. The set point viral load of B*44-positive individuals homozygous for Bw4 was significantly lower than that of B*44-negative individuals homozygous for Bw4 (P= 0.030). The CD4 count declined to <350 in fewer B*44-positive individuals than B*44-negative individuals (X2= 7.295,P= 0.026). B*44-positive individuals had a lower magnitude of p24 pool-specific T cell responses than B*44-negative individuals homozygous for Bw4, though this was not statistically significant. The p24 pool-specific T cell responses were also inversely correlated with lower viral load (rs= −0.88,P= 0.033). Six peptides within p24 were recognized to induce the specific-T cell response in B*44-positive individuals, and the peptide breadth of response was same as that in B*44-negative individuals homozygous for Bw4, but the median magnitude of specific-T cell responses to the recognized peptides in B*44-positive individuals was lower than that in B*44-negative individuals homozygous for Bw4 (P= 0.049). These findings imply that weak p24-specific CD8+T cell responses might play an important role in the control of HIV viremia in B*44 allele-positive individuals. Such studies might contribute to the development of future therapeutic strategies that take into account the genetic background of the patients.

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CD8 T-Cell Recognition of Multiple Epitopes within Specific Gag Regions Is Associated with Maintenance of a Low Steady-State Viremia in Human Immunodeficiency Virus Type 1-Seropositive Patients

Journal of Virology ◽

10.1128/jvi.01847-06 ◽

2006 ◽

Vol 81 (5) ◽

pp. 2440-2448 ◽

Cited By ~ 111

Author(s):

Christof Geldmacher ◽

Jeffrey R. Currier ◽

Eva Herrmann ◽

Antelmo Haule ◽

Ellen Kuta ◽

...

Keyword(s):

Human Immunodeficiency Virus ◽

Steady State ◽

Viral Load ◽

T Cell ◽

Plasma Viral Load ◽

Hla Class I ◽

Cd8 T Cell ◽

Class I ◽

Cell Responses ◽

Immunodeficiency Virus

ABSTRACT The importance of HLA class I-restricted CD8 T-cell responses in the control of human immunodeficiency virus (HIV) infection is generally accepted. While several studies have shown an association of certain HLA class I alleles with slower disease progression, it is not fully established whether this effect is mediated by HIV-specific CD8 T-cell responses restricted by these alleles. In order to study the influence of the HLA class I alleles on the HIV-specific CD8 T-cell response and on viral control, we have assessed HIV-specific epitope recognition, plasma viral load, and expression of HLA class I alleles in a cohort of HIV-seropositive bar workers. Possession of the HLA class I alleles B5801, B8101, and B0702 was associated with a low median viral load and simultaneously with a broader median recognition of Gag epitopes compared to all other HLA alleles (twofold increase) (P = 0.0035). We further found an inverse linear relationship between the number of Gag epitopes recognized and the plasma viral load (R = −0.36; P = 0.0016). Particularly, recognition of multiple epitopes within two regions of Gag (amino acids [aa] 1 to 75 and aa 248 to 500) was associated with the maintenance of a low steady-state viremia, even years after acute infection.

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HLA-C: Plasma viral load and antibiotic susceptibility pattern of microbial infection in HIV-1 among serodiscordant couples in Nigeria

International Journal of Infectious Diseases ◽

10.1016/j.ijid.2020.09.067 ◽

2020 ◽

Vol 101 ◽

pp. 11

Author(s):

N. Otuonye ◽

O. Enabulele ◽

M. Lou ◽

V. Enya ◽

M. Aniedobe ◽

...

Keyword(s):

Viral Load ◽

Antibiotic Susceptibility ◽

Plasma Viral Load ◽

Susceptibility Pattern ◽

Microbial Infection ◽

Serodiscordant Couples ◽

Antibiotic Susceptibility Pattern ◽

Hiv 1

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Correlation of CD4 T Cell Count and Plasma Viral Load with Reproductive Tract Infections/Sexually Transmitted Infections in HIV Infected Females

JOURNAL FOR CLINICAL AND DIAGNOSTIC RESEARCH ◽

10.7860/jcdr/2014/10266.5049 ◽

2014 ◽

Author(s):

Preena Bhalla

Keyword(s):

Viral Load ◽

T Cell ◽

Sexually Transmitted Infections ◽

Plasma Viral Load ◽

Reproductive Tract ◽

Cd4 T Cell ◽

Reproductive Tract Infections ◽

Sexually Transmitted ◽

Tract Infections ◽

Cd4 T Cell Count

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Faculty Opinions recommendation of Higher set point plasma viral load and more-severe acute HIV type 1 (HIV-1) illness predict mortality among high-risk HIV-1-infected African women.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.14292.471794 ◽

2006 ◽

Author(s):

Ann Duerr

Keyword(s):

Viral Load ◽

High Risk ◽

Plasma Viral Load ◽

African Women ◽

Set Point ◽

Acute Hiv ◽

Hiv Type 1 ◽

Hiv 1

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Faculty Opinions recommendation of The major genetic determinants of HIV-1 control affect HLA class I peptide presentation.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.6136957.6362054 ◽

2010 ◽

Author(s):

Thomas Hope ◽

Anna Figueiredo

Keyword(s):

Hla Class I ◽

Class I ◽

Genetic Determinants ◽

Peptide Presentation ◽

Hiv 1

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Proviral HIV-1 DNA in subjects followed since primary HIV-1 infection who suppress plasma viral load after one year of highly active antiretroviral therapy

AIDS ◽

10.1097/00002030-200104130-00001 ◽

2001 ◽

Vol 15 (6) ◽

pp. 665-673 ◽

Cited By ~ 88

Author(s):

Nicole Ngo-Giang-Huong ◽

Christiane Deveau ◽

Isabelle Da Silva ◽

Isabelle Pellegrin ◽

Alain Venet ◽

...

Keyword(s):

Viral Load ◽

Antiretroviral Therapy ◽

Highly Active Antiretroviral Therapy ◽

Plasma Viral Load ◽

Highly Active ◽

One Year ◽

Hiv 1

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Mutually Exclusive T-Cell Receptor Induction and Differential Susceptibility to Human Immunodeficiency Virus Type 1 Mutational Escape Associated with a Two-Amino-Acid Difference between HLA Class I Subtypes

Journal of Virology ◽

10.1128/jvi.01580-06 ◽

2006 ◽

Vol 81 (4) ◽

pp. 1619-1631 ◽

Cited By ~ 64

Author(s):

Xu G. Yu ◽

Mathias Lichterfeld ◽

Senica Chetty ◽

Katie L. Williams ◽

Stanley K. Mui ◽

...

Keyword(s):

Human Immunodeficiency Virus ◽

T Cell ◽

Human Immunodeficiency Virus Type ◽

Virus Type ◽

Hla Class I ◽

Viral Escape ◽

Class I ◽

Immunodeficiency Virus ◽

Hiv 1

ABSTRACT The relative contributions of HLA alleles and T-cell receptors (TCRs) to the prevention of mutational viral escape are unclear. Here, we examined human immunodeficiency virus type 1 (HIV-1)-specific CD8+ T-cell responses restricted by two closely related HLA class I alleles, B*5701 and B*5703, that differ by two amino acids but are both associated with a dominant response to the same HIV-1 Gag epitope KF11 (KAFSPEVIPMF). When this epitope is presented by HLA-B*5701, it induces a TCR repertoire that is highly conserved among individuals, cross-recognizes viral epitope variants, and is rarely associated with mutational escape. In contrast, KF11 presented by HLA-B*5703 induces an entirely different, more heterogeneous TCR β-chain repertoire that fails to recognize specific KF11 escape variants which frequently arise in clade C-infected HLA-B*5703+ individuals. These data show the influence of HLA allele subtypes on TCR selection and indicate that extensive TCR diversity is not a prerequisite to prevention of allowable viral mutations.

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