| |
Increasing incidence of acute hepatitis C in individuals diagnosed with primary HIV in the United Kingdom
|
| |
| |
[Correspondence]
AIDS:Volume 22(5)12 March 2008p 666-668
Fox, Juliea,b; Nastouli, Ea,b; Thomson, Ea,b; Muir, Da,b; McClure, Myraa,b;
Weber, Jonathana,b; Fidler, Saraha,b
aSt Mary's Hospital, London W2 1NY, UK
bImperial College, St Mary's Campus, London W2 1NY, UK.
"We show that individuals with PHI (primary HIV-infection) have higher rates of HCV acquisition than other HIV-positive cohorts [1,2], that HCV acquisition can occur soon after acquiring HIV, and that the incidence of HCV infection is increasing. Consistent with previous studies, the acquisition of HCV was associated with a rise in HIV RNA [9]."
Hepatitis C virus (HCV) is increasingly identified in HIV-positive individuals [1,2]. In a recent study, high-risk sexual behaviour but not intravenous drug use was implicated in HCV acquisition in men who have sex with men (MSM) [3]. The acquisition of HCV in HIV-positive individuals is predominantly asymptomatic [1] and has a deleterious impact on morbidity [4,5]. UK guidelines recommend hepatitis C antibody screening at HIV diagnosis and subsequently according to risk, although risk is not defined [6]. This approach may delay the diagnosis of incident infection permitting unknowing transmission and missed opportunities for early intervention. Primary HIV-1 infection (PHI) is associated with high-risk sexual behaviour and a high frequency of concomitant sexually transmitted infections (STI) [7]. We hypothesized that those diagnosed with PHI may be particularly vulnerable to HCV acquisition.
A total of 155 HIV-1-positive MSM (average age 30 years, range 22-77) identified with PHI (evidence of HIV acquisition within 6 months) were recruited at St Mary's Hospital, London, between1999 and 2006 [8]. Sexual behaviour histories and blood for alanine aminotransferase (ALT) and HCV serology were taken at 3-monthly intervals. Retrospective HCV-RNA polymerase chain reaction testing was carried out on stored serum to determine the approximate time of HCV acquisition.
We found that 11 out of 155 of the men (7%) seroconverted to HCV within this period. The average age of those who acquired HCV was 36 years (range 32-46) (Table 1). The acquisition of HCV occurred year on year from 0/20 in 1999, 0/40 in 2000, 0/65 in 2001, 0/72 in 2002, 0/90 in 2003, 1/40 (2.5%) in 2004, 4/130 (3.1%) in 2005 and 6/155 (3.9%) in 2006.
The median time from PHI diagnosis to the detection of HCV antibody was 23 months (range 8-42); three HCV seroconversions occurred during the first year after PHI, four during the second, two in the third, one in the fourth and one in the fifth. Nine out of 11 individuals were identified with acute HCV after symptoms or having a raised ALT. Two individuals, with admitted high-risk sexual behaviour but normal ALT measurements, were identified by HCV serology.
Retrospective sampling showed that all individuals were HCV-RNA negative at PHI, HCV RNA was detected before antibody detection in four cases and the HCV were of genotypes 1a (eight) and 4d (two). Seven out of 11 individuals had an increase in HIV RNA at HCV seroconversion. There was no association between the HIV-RNA increase and ALT at HCV diagnosis (P = 0.55).
Six out of 11 individuals acquired an STI after PHI, which is significantly higher than in the whole PHI cohort (6/11 versus 26/155; P = 0.004). All acts of unprotected sex occurred with partners of unknown HCV status, whose HIV status was either HIV positive or unknown. All transmissions occurred within the United Kingdom. In the 3 months preceding HCV seroconversion, all denied intravenous drug use, 10 out of 11 had taken recreational drugs, eight reported fisting and four had shared sex toys with casual partners.
Two individuals cleared HCV spontaneously, whereas nine out of 11 remained chronically infected and were offered a one-year course of pegylated interferon α and ribavirin.
We show that individuals with PHI have higher rates of HCV acquisition than other HIV-positive cohorts [1,2], that HCV acquisition can occur soon after acquiring HIV, and that the incidence of HCV infection is increasing. Consistent with previous studies, the acquisition of HCV was associated with a rise in HIV RNA [9].
The higher incidence of STI acquisition in those acquiring HCV highlights the importance of safe sex counselling in HIV-positive individuals. Unprotected sexual contact has grave implications for both the ongoing HIV and the emerging HCV epidemics in MSM. This emphasizes the need for prevention efforts and HCV education among HIV-infected individuals, particularly those reporting high-risk sexual behaviour and recreational drug use. Although 'HIV serosorting' did play a role in the decision to have unprotected sex, serosorting for HCV did not.
This study supports the enhanced surveillance of high-risk groups to identify new HCV cases to prevent the onward transmission of both HCV and HIV and to allow the opportunity for early treatment intervention to enhance HCV clearance rates [8-10]. We recommend the use of targeted sexual behaviour histories in conjunction with regular serum ALT and directed HCV testing. The latter may be particularly valuable to allow early detection in high-risk individuals.
Conflicts of interest: None.
References
1. Browne R, Asboe D, Gilleece Y, Atkins M, Mandalia S, Gazzard B, Nelson M. Increased numbers of acute hepatitis C infections in HIV positive homosexual men; is sexual transmission feeding the increase? Sex Transm Infect 2004; 80:326-327.
2. Turner JM, Rider AT, Imrie J, Copas AJ, Edwards SG, Dodds JP, Stephenson JM, on behalf of the SHARP Study Group. Behavioural predictors of subsequent hepatitis C diagnosis in a UK clinic sample of HIV positive men who have sex with men. Sex Transm Infect 2006; 82:298-300.
3. Danta M, Brown D, Bhagani S, Pybus OG, Sabin CA, Nelson M, et al, for the HIV and Acute HCV (HAAC) Group. Recent epidemic of acute hepatitis C virus in HIV-positive men who have sex with men linked to high-risk sexual behaviours. AIDS 2007; 21:983-991.
4. Greub G, Ledergerber B, Battegay M, Grob P, Perrin L, Furrer H, et al. Clinical progression, survival, and immune recovery during antiretroviral therapy in patients with HIV-1 and hepatitis C virus coinfection: the Swiss HIV Cohort Study. Lancet 2000; 356:1800-1805.
5. Cacoub P, Geffray L, Rosenthal E, Perronne C, Veyssier P, Raguin G. Mortality among HIV-infected patients with cirrhosis or hepatocellular carcinoma due to hepatitis C virus in French Departments of Internal Medicine/Infectious Diseases in 1995 and 1997. Clin Infect Dis 2001; 32:1207-1214.
6. British HIV Association (BHIVA). Guidelines for treatment and management of HIV and hepatitis C co-infection, October 2004. Available at: http://www.bhiva.org/guidelines/2004/HCV/index.html . Accessed: 20 March 2007
7. Pao D, Fisher M, Hue S, Dean G, Murphy G, Cane PA, et al. Transmission of HIV-1 during primary infection: relationship to sexual risk and sexually transmitted infections. AIDS 2005; 19:85-90.
8. Fox J, Dustan S, McClure M, Weber J, Fidler S. Transmitted drug-resistant HIV-1 in primary HIV-1 infection; incidence, evolution and impact on response to antiretroviral therapy. HIV Med 2006; 7:477-483.
9. Gilleece YC, Browne RE, Asboe D, Atkins M, Mandalia S, Bower M, et al. Transmission of hepatitis C virus among HIV-positive homosexual men and response to a 24-week course of pegylated interferon and ribavirin. J Acquir Immune Defic Syndr 2005; 40:41-46.
10. Vogel M, Nattermann J, Baumgarten A, Klausen G, Bieniek B, Schewe K, et al. Pegylated interferon-alpha for the treatment of sexually transmitted acute hepatitis C in HIV-infected individuals. Antivir Ther 2006; 11:1097-1101.
|
|
| |
| |
|
|
|
