scholarly journals Increased Transmission of Vertical Hepatitis C Virus (HCV) Infection to Human Immunodeficiency Virus (HIV)‐Infected Infants of HIV‐ and HCV‐Coinfected Women

1998 ◽  
Vol 178 (4) ◽  
pp. 1047-1052 ◽  
Author(s):  
Vassiliki Papaevangelou ◽  
Henry Pollack ◽  
Gemma Rochford ◽  
Robert Kokka ◽  
Zhiying Hou ◽  
...  
2016 ◽  
Vol 3 (2) ◽  
Author(s):  
Samuel S. Turner ◽  
Sara Gianella ◽  
Marcus J-S. Yip ◽  
Wouter O. van Seggelen ◽  
Robert D. Gillies ◽  
...  

Abstract Background.  The epidemic of sexually transmitted hepatitis C virus (HCV) infection among human immunodeficiency virus (HIV)-infected men who have sex with men (MSM) has been documented for over a decade. Despite this, there is no consensus as to the risk factors for sexual acquisition of HCV in these men. Methods.  We obtained paired semen and blood samples at 2-week intervals from HIV-infected MSM with recent and chronic HCV infection and quantified HCV in semen. Results.  Hepatitis C virus was quantified in 59 semen specimens from 33 men. Hepatitis C virus was shed in 16 (27%) of semen specimens from 11 (33%) of the men. Median HCV viral load (VL) in semen was 1.49 log10 IU/mL. Hepatitis C virus VL in blood was significantly higher at the time of HCV shedding in semen than when HCV shedding in semen was not detected (P = .002). Furthermore, there was a significant correlation between the HCV VL in blood and semen overall (rs = 0.41; P = .001), and in the subgroup with recent HCV infection (rs = 0.37; P = .02), but not in the subgroup with chronic HCV infection (rs = 0.34; P = .1). Conclusions.  One third of HIV-infected MSM coinfected with HCV shed HCV into their semen. Based on the HCV VL in semen in this study, an average ejaculate would deliver up to 6630 IU of virus into the rectum of the receptive partner. Therefore, our data strongly support that condoms should be used during anal intercourse among MSM to prevent transmission of HCV.


Blood ◽  
2004 ◽  
Vol 103 (10) ◽  
pp. 3854-3859 ◽  
Author(s):  
Tomasz Laskus ◽  
Marek Radkowski ◽  
Joanna Jablonska ◽  
Karen Kibler ◽  
Jeffrey Wilkinson ◽  
...  

Abstract Hepatitis C virus (HCV) was found to replicate in monocytes/macrophages particularly in patients with human immunodeficiency virus type 1 (HIV-1) infection. This study was undertaken to determine whether HIV facilitates HCV infection of native human macrophages in vitro. Monocytes/macrophages were collected from healthy donors, infected with HIV M-tropic molecular clone, and then exposed to HCV-positive sera. Presence of positive and negative HCV RNA strands was determined with a novel strand-specific quantitative real-time reverse transcription–polymerase chain reaction (RT-PCR). Preceding as well as near-simultaneous infection with HIV made the macrophages more susceptible to infection with HCV; in particular, an HCV RNA–negative strand was detectable almost exclusively in the setting of concomitant HIV infection. Furthermore, HCV RNAload correlated with HIV replication level in the early stage of infection. The ratio of positive to negative strand in macrophages was lower than in control liver samples. HIV infection was also found to facilitate HCV replication in a Daudi B-cell line with engineered CD4 expression. It seems that HIV infection can facilitate replication of HCV in monocytes/macrophages either by rendering cells more susceptible to HCV infection or by increasing HCV replication. This could explain the presence of extrahepatic HCV replication in HIV-coinfected individuals.


2017 ◽  
Vol 4 (2) ◽  
Author(s):  
Taraz Samandari ◽  
Ellen Tedaldi ◽  
Carl Armon ◽  
Rachel Hart ◽  
Joan S. Chmiel ◽  
...  

Abstract Background There are few recent studies of incident hepatitis C virus (HCV) infection among human immunodeficiency virus (HIV)-infected patients in the United States. Methods We studied HIV Outpatient Study (HOPS) participants seen in 9 HIV-specialty clinics who had ≥1 clinical encounter during 2000–2013 and ≥2 HCV-related tests, the first of which was a negative HCV antibody test (Ab). Hepatitis C virus incident cases were identified by first positive HCV Ab, viral load, or genotype. We assessed rates of incident HCV overall, by calendar intervals, and by demographic and HIV risk strata, and we explored risk factors for incident HCV using Cox proportional hazards models. Results The 1941 eligible patients (median age 40 years, 23% female, 61% men who had sex with men [MSM], and 3% persons who injected drugs [PWID]) experienced 102 (5.3%) incident HCV infections for an overall incidence of 1.07 (95% confidence interval [CI], 0.87–1.30) per 100 person-years (py). Hepatitis C virus incidence decreased from 1.83 in 2000–2003 to 0.88 in 2011–2013 (P = .024), with decreases observed (P < .05) among PWID and heterosexuals, but not among MSM. Overall, MSM comprised 59% of incident cases, and PWID were at most risk for incident HCV infection (adjusted hazard ratio [aHR] for PWID = 4.62 and 95% CI = 2.11–10.13; for MSM, aHR = 1.48 and 95% CI = 0.86–2.55 compared with heterosexuals). Conclusions Among HIV-infected patients in care during 2000–2013, incidence of HCV infection exceeded 1 case per 100 py. Our findings support recommendations for annual HCV screenings for HIV-infected persons, including persons with only MSM risk, to enable HCV diagnosis and treatment for coinfected individuals.


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