scholarly journals Autoantibodies against CD4 cells are associated with CD4 helper defects in human immunodeficiency virus-infected patients

Blood ◽  
1991 ◽  
Vol 77 (1) ◽  
pp. 133-140
Author(s):  
R Weimer ◽  
V Daniel ◽  
R Zimmermann ◽  
K Schimpf ◽  
G Opelz
Keyword(s):  
Human Immunodeficiency Virus ◽  
T Cells ◽  
B Cell ◽  
Hiv Positive ◽  
Cd4 Cells ◽  
T Subsets ◽  
Immunodeficiency Virus ◽  
Hiv Negative ◽  
Autoantibody Formation

To investigate whether autoantibodies against CD4-positive lymphocytes might induce helper dysfunction, autoantibody formation and T-cell function was examined simultaneously in 61 hemophilia patients. Twenty patients were human immunodeficiency virus (HIV)-negative, 26 HIV- positive stage CDC II or III, and 15 were HIV-positive stage CDC IV. T lymphocytes, CD4-positive, or CD8-positive T subsets were cocultured with B lymphocytes and pokeweed mitogen (PWM) for 6 days and Ig- secreting cells were assessed in a reverse hemolytic plaque assay. The presence of IgM, IgG, C3d, or gp120 on the surface of T cells or T subsets was analyzed by flow cytometry. Autoantibodies against CD4- positive T cells were not detected in controls or HIV-negative patients, but were common in HIV-positive patients (20 of 41 patients). In patients with autoantibodies we found an increased incidence of CD4 helper defects (P less than .0001 in CDC II or III patients; P less than .02 in CDC IV patients). 12 of 13 patients with IgM autoantibodies and 4 of 4 with IgG autoantibodies showed CD4 helper defects. Complement fixation had no relevance. Autoantibody formation against CD4 cells was not due to increased in vivo B-cell stimulation (spontaneous plaque formation: 611 +/- 204 PFC/10(6) B cells in autoantibody-negative patients v 650 +/- 202 PFC/10(6) B cells in autoantibody-positive patients; not significant). Thus, our results suggest that autoantibody formation is not caused by a general state of in vivo B-cell activation. Rather, the production of autoantibodies appears to coincide with defects in B-cell proliferation or differentiation, as shown by reduced mitogen-stimulated B-cell responses in CDC II and III patients (P less than .05). Autoantibodies against CD4 cells appear to be involved in the pathogenesis of CD4 helper defects of HIV-infected patients.

scholarly journals Autoantibodies against CD4 cells are associated with CD4 helper defects in human immunodeficiency virus-infected patients

Blood ◽  
1991 ◽  
Vol 77 (1) ◽  
pp. 133-140 ◽  
Author(s):  
R Weimer ◽  
V Daniel ◽  
R Zimmermann ◽  
K Schimpf ◽  
G Opelz
Keyword(s):  
Human Immunodeficiency Virus ◽  
T Cells ◽  
B Cell ◽  
Hiv Positive ◽  
Cd4 Cells ◽  
T Subsets ◽  
Immunodeficiency Virus ◽  
Hiv Negative ◽  
Autoantibody Formation

Abstract To investigate whether autoantibodies against CD4-positive lymphocytes might induce helper dysfunction, autoantibody formation and T-cell function was examined simultaneously in 61 hemophilia patients. Twenty patients were human immunodeficiency virus (HIV)-negative, 26 HIV- positive stage CDC II or III, and 15 were HIV-positive stage CDC IV. T lymphocytes, CD4-positive, or CD8-positive T subsets were cocultured with B lymphocytes and pokeweed mitogen (PWM) for 6 days and Ig- secreting cells were assessed in a reverse hemolytic plaque assay. The presence of IgM, IgG, C3d, or gp120 on the surface of T cells or T subsets was analyzed by flow cytometry. Autoantibodies against CD4- positive T cells were not detected in controls or HIV-negative patients, but were common in HIV-positive patients (20 of 41 patients). In patients with autoantibodies we found an increased incidence of CD4 helper defects (P less than .0001 in CDC II or III patients; P less than .02 in CDC IV patients). 12 of 13 patients with IgM autoantibodies and 4 of 4 with IgG autoantibodies showed CD4 helper defects. Complement fixation had no relevance. Autoantibody formation against CD4 cells was not due to increased in vivo B-cell stimulation (spontaneous plaque formation: 611 +/- 204 PFC/10(6) B cells in autoantibody-negative patients v 650 +/- 202 PFC/10(6) B cells in autoantibody-positive patients; not significant). Thus, our results suggest that autoantibody formation is not caused by a general state of in vivo B-cell activation. Rather, the production of autoantibodies appears to coincide with defects in B-cell proliferation or differentiation, as shown by reduced mitogen-stimulated B-cell responses in CDC II and III patients (P less than .05). Autoantibodies against CD4 cells appear to be involved in the pathogenesis of CD4 helper defects of HIV-infected patients.

Abstract WP426: Subarachnoid Hemorrhage in patients infected with Human Immunodeficiency Virus

Stroke ◽  
2013 ◽  
Vol 44 (suppl_1) ◽  
Author(s):  
Haralabos Zacharatos ◽  
Malik M Adil ◽  
Ameer E Hassan ◽  
Sarwat I Gilani ◽  
Adnan I Qureshi
Keyword(s):  
Human Immunodeficiency Virus ◽  
Subarachnoid Hemorrhage ◽  
Blood Transfusion ◽  
Hospital Mortality ◽  
Hiv Infection ◽  
The United States ◽  
Hiv Positive ◽  
Published Data ◽  
Immunodeficiency Virus ◽  
Hiv Negative

Background: There is limited data regarding the unique attributes of ischemic stroke among patients infected with human immunodeficiency virus (HIV). There is no published data regarding the occurrence and outcomes of subarachnoid hemorrhage (SAH) among HIV infected persons. Methods: The largest all-payer Nationwide Inpatient Sample (NIS 2002-2010) data was used to identify and analyze all patients presenting with the primary diagnosis of SAH in the United States. Among this cohort, we identified the patients who were not HIV positive and those who were HIV positive. Patient demographics, medical co-morbidities, in-hospital complications, in-hospital procedures, and discharge disposition were compared between the two groups. The association between HIV infection and outcomes was evaluated in multivariate analysis after adjusting for potential confounders. Results: Of the 351,491 patients admitted with SAH, 1367 (0.39%) were infected with HIV. HIV infected patients were younger, mean age [±SD] of 45 ±14.2 years versus those who were not 58±19 years, (p<0.0001). The rate of blood transfusion [27,286 (7.8%) versus 245.6 (18%), p=0.0003], mechanical ventilation [51,199 (14.6%) versus 316.1(23.1%), p=0.008], and sepsis [14,644 (4.2%) versus 236.1 (17.3%), p<0.0001] was significantly higher among HIV infected patients. After adjusting for age, gender, hypertension, coagulopathy, atrial fibrillation, renal failure, and dyslipidemia, HIV negative patients had a significantly higher rate of discharge to home (odds ratio [OR] 1.9, 95% CI: 1.4-2.6, p<0.0001) and lower in-patient mortality (OR 0.4, 95% CI: 0.3-0.5, p<0.001). Further adjustment for blood transfusion and sepsis reduced the odds of discharge to home for the HIV negative patients, from 1.9 to 1.7 but did not affect in-hospital mortality. Conclusion: The in-hospital mortality in HIV infected patients with SAH is higher despite these patients being younger than non-HIV infected patients. We believe that this study provides a nationwide perspective which may have some important implications for early recognition and diagnosis of HIV-infection in SAH patients.

Antimalarial drug resistance markers in human immunodeficiency virus (HIV)-positive and HIV-negative adults with asymptomatic malaria infections in Port Harcourt, Nigeria

2021 ◽  
Author(s):  
Ifeyinwa Chijioke-Nwauche ◽  
Mary C Oguike ◽  
Chijioke A Nwauche ◽  
Khalid B Beshir ◽  
Colin J Sutherland
Keyword(s):  
Human Immunodeficiency Virus ◽  
Drug Resistance ◽  
Drug Susceptibility ◽  
Blood Film ◽  
University Hospital ◽  
Hiv Positive ◽  
Asymptomatic Malaria ◽  
Immunodeficiency Virus ◽  
Before And After ◽  
Hiv Negative

Abstract Background In Nigeria, indiscriminate use of antimalarial drugs may contribute to the threat of drug resistance, but this has not been evaluated among people living with human immunodeficiency virus (HIV). Methods HIV-positive adults attending a university hospital HIV clinic and HIV-negative adult volunteers from the university hospital community with a positive blood film were treated with artemether–lumefantrine. Parasite DNA from before and after treatment was polymerase chain reaction amplified to identify molecular markers of drug susceptibility. Results The pfcrt76T genotype was prevalent among both HIV-positive and HIV-negative participants (78.6% and 68.2%, respectively). Three new mutations in the pfmdr1 gene—F73S, S97L and G165R—and the uncommon pfdhps S436F variant were detected, whereas pfdhps K540E and pfdhfr I164L were absent. The A437G allele of pfdhps predominated (62/66 [94%]). The I431 V mutation was found in 19 of 66 pretreatment pfdhps sequences (28.8%). The pfmdr1 86N allele was significantly more common at day 3 post-treatment than at baseline (odds ratio 8.77 [95% confidence interval 1.21 to 380]). Conclusions We found evidence of continued chloroquine use among HIV-positive individuals. Selection for the pfmdr1 86N after artemether–lumefantrine treatment was observed, indicating a possible threat to antimalarial efficacy in the study area. The complexity of pfdhps haplotypes emphasises the need for careful monitoring of anti-folate susceptibility in Nigeria.

Trypanosoma cruziParasitemia in Chronic Chagas Disease: Comparison between Human Immunodeficiency Virus (HIV)–Positive and HIV‐Negative Patients

2002 ◽  
Vol 186 (6) ◽  
pp. 872-875 ◽  
Author(s):  
Ana Marli C. Sartori ◽  
José Eluf Neto ◽  
Elizabete Visone Nunes ◽  
Lucia Maria Almeida Braz ◽  
Hélio H. Caiaffa‐Filho ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Chagas Disease ◽  
Hiv Positive ◽  
Immunodeficiency Virus ◽  
Chronic Chagas Disease ◽  
Hiv Negative

scholarly journals Human immunodeficiency virus (HIV) Tat-reactive antibodies present in normal HIV-negative sera and depleted in HIV-positive sera. Identification of the epitope.

1992 ◽  
Vol 175 (5) ◽  
pp. 1247-1253 ◽  
Author(s):  
T C Rodman ◽  
F H Pruslin ◽  
S E To ◽  
R Winston
Keyword(s):  
Human Immunodeficiency Virus ◽  
Natural Antibodies ◽  
Hiv Positive ◽  
Tat Protein ◽  
Very High Frequency ◽  
Hiv Pathogenesis ◽  
Humoral Immune ◽  
Igm Antibodies ◽  
Immunodeficiency Virus ◽  
Hiv Negative

We have detected, in sera of normal human immunodeficiency virus (HIV)-free subjects, IgM antibodies reactive with the Tat protein of HIV in significant titers and at very high frequency, and, in HIV-positive sera, progressively lower titers as HIV pathogenesis ensues. Epitope analysis indicates that the Tat-reactive antibodies of both HIV-negative and HIV-positive sera are homologous, suggesting, therefore, that their decline in HIV-positive sera may represent attrition of a host defense factor. The identified epitope displays minimal homology with that previously defined for another set of IgM antibodies shown to be present in normal sera, deficient in HIV-positive sera, and postulated to be natural antibodies. We propose that the Tat-reactive antibodies, as well, are a set of natural antibodies and that the normal humoral immune system includes a repertoire of antibodies, nonimmunogenic in origin, that contribute to immune homeostasis and, consequently, to host resistance to HIV pathogenesis.

scholarly journals Potent activity of 2'-beta-fluoro-2',3'-dideoxyadenosine against human immunodeficiency virus type 1 infection in hu-PBL-SCID mice.

1996 ◽  
Vol 40 (10) ◽  
pp. 2369-2374 ◽  
Author(s):  
K Ruxrungtham ◽  
E Boone ◽  
H Ford ◽  
J S Driscoll ◽  
R T Davey ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
T Cells ◽  
Hiv Infection ◽  
Infection Rate ◽  
Cd4 T Cells ◽  
Scid Mice ◽  
Immunodeficiency Virus ◽  
Anti Hiv

A new antiretroviral agent, 2'-beta-fluoro-2',3'-dideoxyadenosine (FddA), is an acid-stable compound whose triphosphate form is a potent reverse transcriptase inhibitor with in vitro anti-human immunodeficiency virus (HIV) activity and a favorable pharmacokinetic profile. Severe combined immunodeficiency (SCID) mice reconstituted with human peripheral blood leukocytes (hu-PBL-SCID mice) provide a useful small-animal model for HIV research. In the present study we utilized this experimental system for the in vivo evaluation of the anti-HIV activity of this new compound when administered prior to infection. Initial studies revealed that, following a challenge with 50 100% tissue culture infective doses of HIV type 1 lymphadenopathy-associated virus, 39 of 42 (93%) control mice developed HIV infection, as evidenced by positive coculture or positive PCR. Administration of zidovudine decreased the infection rate to 5 of 16 (31%), while administration of FddA decreased the infection rate to 0 of 44 (0%). In follow-up controlled studies, the anti-HIV activity of FddA was confirmed, with 18 of 20 control mice showing evidence of HIV infection, compared with 4 of 20 FddA-treated mice. In addition to having direct anti-HIV effects, FddA was found to have a protective effect on human CD4+ T cells in the face of HIV infection. Mice treated with FddA were found to have a significantly higher percentage of CD4+ T cells than controls (10.3% +/- 3.4% versus 0.27% +/- 0.21%; P = 0.01). Thus, FddA, with its potent anti-HIV activity in vivo, high oral bioavailability, long intracellular half-life, and ability to preserve CD4+ cells in the presence of HIV, appears to be a promising agent for clinical investigation.

scholarly journals CD4-Negative Cells Bind Human Immunodeficiency Virus Type 1 and Efficiently Transfer Virus to T Cells

2000 ◽  
Vol 74 (18) ◽  
pp. 8550-8557 ◽  
Author(s):  
Gene G. Olinger ◽  
Mohammed Saifuddin ◽  
Gregory T. Spear
Keyword(s):  
Human Immunodeficiency Virus ◽  
T Cells ◽  
Mononuclear Cells ◽  
Cell Types ◽  
Virus Binding ◽  
Peripheral Blood Mononuclear ◽  
Human Immunodeficiency Virus Strain ◽  
Immunodeficiency Virus

ABSTRACT The ability of human immunodeficiency virus strain MN (HIVMN), a T-cell line-adapted strain of HIV, and X4 and R5 primary isolates to bind to various cell types was investigated. In general, HIVMN bound to cells at higher levels than did the primary isolates. Virus bound to both CD4-positive (CD4+) and CD4-negative (CD4−) cells, including neutrophils, Raji cells, tonsil mononuclear cells, erythrocytes, platelets, and peripheral blood mononuclear cells (PBMC), although virus bound at significantly higher levels to PBMC. However, there was no difference in the amount of HIV that bound to CD4-enriched or CD4-depleted PBMC. Virus bound to CD4− cells was up to 17 times more infectious for T cells in cocultures than was the same amount of cell-free virus. Virus bound to nucleated cells was significantly more infectious than virus bound to erythrocytes or platelets. The enhanced infection of T cells by virus bound to CD4− cells was not due to stimulatory signals provided by CD4− cells or infection of CD4− cells. However, anti-CD18 antibody substantially reduced the enhanced virus replication in T cells, suggesting that virus that bound to the surface of CD4−cells is efficiently passed to CD4+ T cells during cell-cell adhesion. These studies show that HIV binds at relatively high levels to CD4− cells and, once bound, is highly infectious for T cells. This suggests that virus binding to the surface of CD4− cells is an important route for infection of T cells in vivo.

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