byline: Larry: MSM transmission and case definition of HCV in AID...

byline: Larry: MSM transmission and case definition of HCV in AID...: " The European AIDS Treatment Network (NEAT) Acute Hepatitis CInfection Consensus PanelJu¨rgen K. Rockstroh (excerpts) (1) Case definiti..."

MSM transmission and case definition of HCV in AIDS infection.

 

The European AIDS Treatment Network (NEAT) Acute Hepatitis C

Infection Consensus Panel

Ju¨rgen K. Rockstroh

(excerpts)

(1) Case definition and diagnoses

(2) HCV transmission in MSM

(1) Case definition and diagnosis of acute HCV

infection in HIV-infected patients

Case definition and diagnosis of acute HCV infection in HIV-infected patientsAcute hepatitis C virus (HCV) infection is defined as the first six months after exposure to HCV. This definition is arbitrary as there is a lack of evidence on when ‘acute’ infection becomes ‘chronic’ and determining the precise timing of infection is usually problematic. As the majority of individuals with acute HCV infection are asymptomatic clinical diagnosis has a low sensitivity.  Differentiating between acute HCV infection and an exacerbation of chronic HCV infection clinically, virologically and immunologically is difficult in the absence of recent negative HCV RNA and antibody results. A serological test does not exist to differentiate between acute and chronic infection.  One third to a half of individuals with acute HCV infection experience symptoms attributable to an acute illness, although symptoms are non-specific.  The first marker of HCV infection is serum or plasma HCV RNA detected via nucleic acid test (NAT) as early as one week post infection. HCV antibody responses may be delayed or absent in HIV-infected individuals with two thirds positive at three months and 5% remaining negative up to one year after infection.  Fluctuations in HCV-RNA levels during the acute phase of HCV infection are characteristic in HIV-uninfected  individuals and may be of value in suggesting a diagnosis of acute hepatitis C.

  

(2) HCV transmission in MSM

Studies in MSM have shown HIV infection and intravenous drug use to be independently associated with the presence of HCVantibodies. In early reports, evidence for sexual transmission was weak with conflicting evidence of an association with sexual risk behaviour.  Recent studies investigating factors underlying HCV transmission in HIV-infected MSM have provided further evidence for an association with certain sexual practices including fisting, using sex toys, and group sex.  Non-injecting drug use is also associated, probably because of the influence on sexual behaviour but transmission through sharing contaminated devices may also contribute. There is an association with bacterial sexually transmitted infections notably syphilis and lymphogranuloma venereum. The mechanism of sexual transmission remains uncertain but the association with traumatic sexual practices and ulcerative STIs affecting the mucosa of the rectum provides some clues. HCV RNA has been detected in semen and more often in the HIV-infected, although one study failed to detect HCV RNA in the semen of most HIV-infected men even during acute HCV infection. Group sex may facilitate transfer of infected material. Other causes of disruption of the ano-rectal mucosa, including surgery, may contribute to the risk. There is no evidence that HIV-infected men are more susceptible to HCV infection due to immunological deficits, or that a more virulent HCV strain is being selected.  Phylogenetic analyses of transmitted HCV strains show clustering consistent with transmission among a social and sexual network of HIV-infected MSM, which extends nationally and internationally. Although the majority of patients present with two or more risk factors described above, cases of acute HCV infection are seen in MSM who report only unprotected anal intercourse. Although current outbreaks have been largely confined to HIVinfected MSM, cases have also been reported in HIV-uninfected individuals.5 ULN in less than 2 % [9], minimizing the possibility of classifying ‘‘chronic’’ HCV infection as ‘‘acute’’. The first marker of HCV infection is serum or plasma HCV RNA detected via nucleic acid test (NAT) as early as one week post infection.  HCV antibody responses may be delayed or absent in HIV-infected individuals with two thirds positive at three months and 5% remaining negative up to one year after infection. Fluctuations in HCV-RNA levels during the acute phase of HCV infection are characteristic in HIV-uninfected individuals and may be of value in suggesting a diagnosis of acute hepatitis C 

Acute hepatitis C in HIV-infected individuals –

recommendations from the NEAT

consensus conference