Alcohol Intake Increases Human Immunodeficiency Virus Type 1 Replication in Human Peripheral Blood Mononuclear Cells

Bagasra, Omar; Balla, Andre; Lischner, Harold W.; Pomerantz, Roger J.

doi:10.1093/infdis/167.4.789

Cited by 95 publications

(57 citation statements)

References 32 publications

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“…[32][33][34][35][36] Our study showed significantly higher levels of HIV-1 p24 in the plasma of hu-PBL-NOD/ SCID HIVE mice chronically exposed to ethanol as compared to controls fed an isocaloric diet (Table 2). Although the effects of ethanol on HIV-1 infection still remain inconclusive, our results parallel observations in which chronic alcohol exposure in macaques infected with simian immunodeficiency virus (animal model for HIV-1 infection) resulted in high plasma viral load.…”

Section: Discussionmentioning

confidence: 99%

Alcohol Abuse Enhances Neuroinflammation and Impairs Immune Responses in an Animal Model of Human Immunodeficiency Virus-1 Encephalitis

Potula

Haorah

Knipe

et al. 2006

The American Journal of Pathology

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Section: Discussionmentioning

confidence: 99%

Alcohol Abuse Enhances Neuroinflammation and Impairs Immune Responses in an Animal Model of Human Immunodeficiency Virus-1 Encephalitis

Potula

Haorah

Knipe

et al. 2006

The American Journal of Pathology

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“…For example, alcohol intake has been shown to increase human immunodeficiency virus replication in human peripheral blood mononuclear cells in culture. 13 The T lymphocyte system seems to be extensively affected by alcohol. There might be a transient immunosuppressive environment in which viruses (HIV and, possibly, HCV) replicate faster than in intact immune sytem.…”

Section: Discussionmentioning

confidence: 99%

“…[11][12] Moreover relations between alcohol and the immune response have been suggested with other viral infections. 13 The aim of the present study is to describe the effect of moderate alcohol intake on serum HCV RNA levels and histological liver lesions in patients with chronic HCV infection. …”

mentioning

confidence: 99%

Effect of alcohol consumption on serum hepatitis C virus RNA and histological lesions in chronic hepatitis C

et al. 1998

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The role of alcohol intake in the occurrence of severe liver disease in chronic hepatitis C virus (HCV) carriers is still debated. A cross-sectional study has been conducted in 233 chronic hepatitis C virus carriers. Weekly self-reported alcohol consumption (SRAC) was evaluated, serum HCV RNA levels were measured by a branched DNA technique (Quantiplex 2.0) and HCV genotypes were determined. A liver biopsy was performed simultaneously and liver lesions were graded with the Knodell histological activity index. Data were examined by uni-and multivariate analyses. Alcohol consumption was relatively low (F 140 g/per week in 193/233 patients [80%]). We found a highly significant correlation between SRAC and serum HCV RNA levels (r ‫؍‬ .26, P ‫؍‬ .001). Fibrosis was significantly correlated with age and alcohol consumption. These results suggest that in HCV carriers, alcohol consumption, even with low alcohol intake, increases viremia and hepatic fibrosis. Chronic HCV carriers should be advised to avoid regular alcohol intake. (HEPATOLOGY 1998;27:1717-1722.)The natural course of HCV infection is probably modulated by several cofactors. The role of virus-related factors, namely genotypes and viremia has been extensively studied 1-7 but still remains debated. 8 Up to now, immunological factors were underestimated but several arguments implicate the role of immune response in the course of the disease. Environmental factors and particularly alcohol intake are probably major factors, 9-10 and the increased severity of the disease and the faster occurrence of cirrhosis in patients with HCV infection and heavy alcohol intake has been suggested in several studies. [11][12] Moreover relations between alcohol and the immune response have been suggested with other viral infections. 13 The aim of the present study is to describe the effect of moderate alcohol intake on serum HCV RNA levels and histological liver lesions in patients with chronic HCV infection.

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“…Suppressed T-cell proliferation caused by retrovirus infection was significantly reduced further by dietary alcohol [195]. Although alcohol had no effect on the relative production of CD4 þ and CD8 þ lymphocytes, reductions of lymphocyte-produced IL-2 and of the soluble immune response activity of suppressor cells occurred [196]. Alcohol consumption suppresses IFN-production by human peripheral blood lymphocytes [197] and antiviral CD8 þ T cells [128].…”

Section: Alcohol and Innate Immunitymentioning

confidence: 99%

Drug abuse, innate immunity and hepatitis C virus

Zhang

2006

Reviews in Medical Virology

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Since its discovery in 1989, hepatitis C virus (HCV) has become a major public health problem. HCV chronically infects an estimated 170 million people worldwide. The seroprevalence of anti-HCV antibody in the United States has been estimated at 1.8%, which corresponds to approximately 4 million people. HCV is the most common chronic blood borne infection in the United States, and the leading cause of liver transplantation in developed countries. Injection drug use is the dominant mode of HCV transmission and accounts for up to 90% of current infections. Opiates and other drug abuse, such as alcohol, have been implicated as cofactors in the pathogenesis of HCV disease. Injection drug use has been the most common risk factor identified in alcoholics with HCV infection. Both opiates and alcohol contribute significantly to morbidity and mortality from HCV disease. These drugs most likely act synergistically to promote the development and progression of HCV disease. However, there is limited information available concerning the interaction of the drug abuse with the host cell innate immunity against HCV infection, which is a major barrier to fundamental understanding of the immunopathogenesis of HCV disease. Therefore, defining the role of the drug abuse in the development of chronic HCV infection is of crucial importance and should provide practical guidance toward the reduction of risk factors that interfere with therapeutic approaches for HCV infection and disease. This review paper focuses on the interplay between drug abuse (opiates and alcohol), innate immunity and HCV in the context of the development of HCV disease.

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Alcohol Intake Increases Human Immunodeficiency Virus Type 1 Replication in Human Peripheral Blood Mononuclear Cells

Cited by 95 publications

References 32 publications

Alcohol Abuse Enhances Neuroinflammation and Impairs Immune Responses in an Animal Model of Human Immunodeficiency Virus-1 Encephalitis

Alcohol Abuse Enhances Neuroinflammation and Impairs Immune Responses in an Animal Model of Human Immunodeficiency Virus-1 Encephalitis

Effect of alcohol consumption on serum hepatitis C virus RNA and histological lesions in chronic hepatitis C

Drug abuse, innate immunity and hepatitis C virus

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