HIV-1 Infection, Neuroendocrine Abnormalities, and Clinical Outcomes

CNS Spectrums ◽  
2000 ◽  
Vol 5 (5) ◽  
pp. 55-65 ◽  
Author(s):  
Mahendra Kumar ◽  
Karl Goodkin ◽  
Adarsh M. Kumar ◽  
Teri T. Baldewicz ◽  
Robert Morgan ◽  
...  
Keyword(s):  
Needle Aspiration ◽  
Future Research ◽  
Major Life ◽  
Immunodeficiency Virus ◽  
Life Stressor ◽  
Acquired Immunodeficiency ◽  
Immunodeficiency Syndrome ◽  
Hiv 1 ◽  
Neuroendocrine Systems

AbstractDifferent lines of evidence suggest that human immunodeficiency virus type 1 (HIV-1) infection is complicated by a variety of adverse effects on neuroendocrine systems. Soon after the discovery of HIV-1, reports began to appear suggesting that a number of neurotransmitter and neuroendocrine activities were negatively impacted by this infection. In 1987 it was observed that fine-needle aspiration of the lung in patients with acquired immunodeficiency syndrome resulted in syncopal reactions. Subsequently, an abnormality in the autonomic nervous system was reported in these patients. However, investigations in this area have remained limited due to the assumption that HIV-1–mediated activation of various endocrine systems was related to the major life stressor of living with a fatal disease. Evidence accumulated over the years has indicated, instead, that there are various other mechanisms in addition to life stressors that also play an important role in negatively impacting the neuroendocrine systems in this infection. This article examines various developments that have taken place in this area in order to provide avenues for future research.

Detection of HIV Antibody and Antigen (p24) in Residual Blood on Needles and Glass

1990 ◽  
Vol 11 (4) ◽  
pp. 180-184 ◽  
Author(s):  
Djamshid Shirazian ◽  
Barry C. Herzlich ◽  
Foroozan Mokhtarian ◽  
David Grob
Keyword(s):  
Western Blot ◽  
Enzyme Linked Immunosorbent Assay ◽  
Immunodeficiency Virus ◽  
Circulating Antigen ◽  
Acquired Immunodeficiency ◽  
Residual Blood ◽  
The Individual ◽  
Immunodeficiency Syndrome ◽  
Hiv 1

AbstractThere is a significant rate of percutaneous injury with needles during the care of patients with acquired immunodeficiency syndrome (AIDS). Following puncture injury, it is recommended that the source of the contaminating blood be checked, and if human immunodeficiency virus-type 1- (HIV-1)-seropositive, zidovudine prophylaxis be considered. As the source of contaminating blood may be unknown, we studied the detectability of HIV-1 antibody and circulating antigen (p24) in the residual blood from needles and pieces of glass at various intervals following exposure to blood. The residual volume of blood remaining in needles varied from 183 ±50 μ 1 for a 20 G needle to 7.8 ± 1 μ 1 for a 27 G needle, and the residual blood on small pieces of glass varied from 23 μ 1 for a piece weighing 558 mg to 2 μ 1 for a piece weighing 21 mg. Analysis of washed samples of residual blood from all 20 G through 26 G needles and from broken pieces of glass larger than 0.41 g that had been exposed to HIV-1-seropositive blood and left at room temperature for one hour, one day and one week resulted in positive tests for HIV-1 antibody by enzyme-linked immunosorbent assay (ELISA), immunofluorescence and Western blot assays. The circulating antigen was detected in residual blood of 20 G through 26 G needles, but not from contaminated pieces of glass. This technique could be applied to situations where a healthcare worker pricked him- or herself with a needle or with a piece of glass that had been contaminated with blood of unknown seroreactivity. If HIV-1 ELISA, immunofluorescence, Western blot and circulating antigen assays are negative, the individual can be reassured. Because only 0.4% of needlestick injuries with HIV-1-seropositive blood have resulted in seroconversion, there must be other factors, as yet unknown, that predispose to infection.

scholarly journals Acquired immunodeficiency syndrome-associated T-cell lymphoma: evidence for human immunodeficiency virus type 1-associated T-cell transformation

Blood ◽  
1992 ◽  
Vol 79 (7) ◽  
pp. 1768-1774 ◽  
Author(s):  
BG Herndier ◽  
BT Shiramizu ◽  
NE Jewett ◽  
KD Aldape ◽  
GR Reyes ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
T Cell ◽  
B Cell ◽  
Virus Type ◽  
Cell Lymphoma ◽  
Immunodeficiency Virus ◽  
Acquired Immunodeficiency ◽  
Immunodeficiency Syndrome ◽  
Hiv 1

Abstract The majority of lymphomas in the setting of acquired, iatrogenic, or congenital immunodeficiencies are B-cell lymphoproliferations. We describe a rare T-cell lymphoma in a fulminantly ill patient infected with human immunodeficiency virus type 1 (HIV-1). The T-cell nature of the process was defined genotypically (monoclonal T-cell receptor beta- chain [CT beta] rearrangement) and phenotypically (CD45RO+, CD4+, CD5+, CD25+, CD8-, CD3- and negative for a variety of B-cell and monocyte markers). The CD4+, CD25+ (interleukin-2 receptor [IL-2R]) phenotype with production of IL-2 and IL-2R RNA is analogous to human T- lymphotropic virus type I (HTLV-I)-associated adult T-cell leukemia/lymphoma (ATLL); however, no HTLV-1 could be detected. Southern blot analysis did demonstrate monoclonally integrated HIV-1 within the tumor genome. Furthermore, the tumor cells were producing HIV p24 antigen as shown by immunohistochemistry. This is the first case of acquired immunodeficiency syndrome (AIDS)-associated non- Hodgkin's lymphoma in which HIV-1 infection may have played a central role in the lymphocyte transformation process.

scholarly journals Acquired immunodeficiency syndrome-associated T-cell lymphoma: evidence for human immunodeficiency virus type 1-associated T-cell transformation

Blood ◽  
1992 ◽  
Vol 79 (7) ◽  
pp. 1768-1774 ◽  
Author(s):  
BG Herndier ◽  
BT Shiramizu ◽  
NE Jewett ◽  
KD Aldape ◽  
GR Reyes ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
T Cell ◽  
B Cell ◽  
Virus Type ◽  
Cell Lymphoma ◽  
Immunodeficiency Virus ◽  
Acquired Immunodeficiency ◽  
Immunodeficiency Syndrome ◽  
Hiv 1

The majority of lymphomas in the setting of acquired, iatrogenic, or congenital immunodeficiencies are B-cell lymphoproliferations. We describe a rare T-cell lymphoma in a fulminantly ill patient infected with human immunodeficiency virus type 1 (HIV-1). The T-cell nature of the process was defined genotypically (monoclonal T-cell receptor beta- chain [CT beta] rearrangement) and phenotypically (CD45RO+, CD4+, CD5+, CD25+, CD8-, CD3- and negative for a variety of B-cell and monocyte markers). The CD4+, CD25+ (interleukin-2 receptor [IL-2R]) phenotype with production of IL-2 and IL-2R RNA is analogous to human T- lymphotropic virus type I (HTLV-I)-associated adult T-cell leukemia/lymphoma (ATLL); however, no HTLV-1 could be detected. Southern blot analysis did demonstrate monoclonally integrated HIV-1 within the tumor genome. Furthermore, the tumor cells were producing HIV p24 antigen as shown by immunohistochemistry. This is the first case of acquired immunodeficiency syndrome (AIDS)-associated non- Hodgkin's lymphoma in which HIV-1 infection may have played a central role in the lymphocyte transformation process.

INFLUENCE OF HOST GENOTYPE ON PROGRESSION TO ACQUIRED IMMUNODEFICIENCY SYNDROME AMONG CHILDREN INFECTED WITH HUMAN IMMUNODEFICIENCY VIRUS TYPE 1

PEDIATRICS ◽  
1996 ◽  
Vol 98 (2) ◽  
pp. 348-348
Author(s):  
Joseph A. Church
Keyword(s):  
Clinical Course ◽  
Host Factors ◽  
Host Genotype ◽  
Immunodeficiency Virus ◽  
Acquired Immunodeficiency ◽  
Specific Factors ◽  
Immunodeficiency Syndrome ◽  
Clinical Pictures ◽  
Hla Genotype

The specific factors that determine the clinical course in individual patients with HIV infection are yet to be precisely defined. Variable virus subtypes are likely to produce different clinical pictures. This article documents that host factors, such as HLA genotype, are also important in clinical outcome. The relative importance of host versus viral characteristics is as yet undetermined.

scholarly journals PARAMETER OPTIMIZATION AND VIRTUAL SCREENING INDONESIAN HERBAL DATABASE AS HUMAN IMMUNODEFICIENCY VIRUS -1 INTEGRASE INHIBITOR USING AUTODOCK AND VINA

2017 ◽  
Vol 9 ◽  
pp. 90
Author(s):  
Arry Yanuar ◽  
Rezi Riadhi Syahdi ◽  
Widya Dwi Aryati
Keyword(s):  
Human Immunodeficiency Virus ◽  
Virtual Screening ◽  
Integrase Inhibitor ◽  
Water Molecules ◽  
Autodock Vina ◽  
Unit Space ◽  
Immunodeficiency Virus ◽  
Acquired Immunodeficiency ◽  
Immunodeficiency Syndrome ◽  
Hiv 1

Objective: Human immunodeficiency virus (HIV-1) is a virus that causes acquired immunodeficiency syndrome, a disease considered to be one of themost dangerous because of its high mortality, morbidity, and infectivity. The emergence of mutant HIV strains has led treatment to target proteaseas reverse transcriptase and integrase enzyme become less effective. This study aims to provide knowledge about the potential of HIV-1 integraseinhibitors for use as guiding compounds in the development of new anti-HIV drugs.Methods: This study used AutoDock and AutoDock Vina for virtual screening of the Indonesian herbal database for inhibitors of HIV-1 integrase andis validated using a database of the directory of useful decoys. Optimization was accomplished by selecting the grid size, the number of calculations,and the addition of two water molecules and a magnesium atom as cofactor.Results: This study determined that the best grid box size is 21.1725×21.1725×21.1725 in unit space size (1 unit space equals to macromolecules 1Ǻ),using AutoDock Vina with EF and AUC values, 3.93 and 0.693, respectively. Three important water molecules have meaning in molecular dockingaround the binding pocket.Conclusions: This study obtained the top ten ranked compounds using AutoDock Vina. The compounds include: Casuarinin; Myricetin-3-O-(2’’,6’’-di-O-α-rhamnosyl)-β-glucoside; 5,7,2’,4’-tetrahydroxy-6,3’-diprenylisoflavone 5-O-(4’’-rhamnosylrhamnoside); myricetin 3-robinobioside; cyanidin3-[6-(6-ferulylglucosyl)-2-xylosylgalactoside]; mesuein, cyanidin 7-(3-glucosyl-6-malonylglucoside)-4’-glucoside; kaempferol 3-[glucosyl-(1→3)-rhamnosyl-(1→6)-galactoside]; 3-O-galloylepicatechin-(4-β→8)-epicatechin-3-O-gallate; and quercetin 4’-glucuronide.

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