Occupational Transmission of HCV

Risk for Occupational Transmission of HCV

HCV is not transmitted efficiently through occupational exposures to blood. The average incidence of anti-HCV seroconversion after accidental percutaneous exposure from an HCV-positive source is 1.8% (range: 0%–7%) (73–76), with one study indicating that transmission occurred only from hollow-bore needles compared with other sharps (75). Transmission rarely occurs from mucous membrane exposures to blood, and no transmission in HCP has been documented from intact or nonintact skin exposures to blood (77,78). Data are limited on survival of HCV in the environment. In contrast to HBV, the epidemiologic data for HCV suggest that environmental contamination with blood containing HCV is not a significant risk for transmission in the health-care setting (79,80), with the possible exception of the hemodialysis setting where HCV transmission related to environmental contamination and poor infection-control practices have been implicated (81–84). The risk for transmission from exposure to fluids or tissues other than HCV-infected blood also has not been quantified but is expected to be low.

In several studies, researchers have attempted to assess the effectiveness of IG following possible exposure to non-A, non-B hepatitis. These studies have been difficult to interpret because they lack uniformity in diagnostic criteria and study design, and, in all but one study, the first dose of IG was administered before potential exposure (48,85,86). In an experiment designed to model HCV transmission by needlestick exposure in the health-care setting, high anti-HCV titer IG administered to chimpanzees 1 hour after exposure to HCV-positive blood did not prevent transmission of infection (87). In 1994, the Advisory Committee on Immunization Practices (ACIP) reviewed available data regarding the prevention of HCV infection with IG and concluded that using IG as PEP for hepatitis C was not supported (88). This conclusion was based on the following facts:

• No protective antibody response has been identified following HCV infection.
• Previous studies of IG use to prevent posttransfusion non-A, non-B hepatitis might not be relevant in making recommendations regarding PEP for hepatitis C.
• Experimental studies in chimpanzees with IG containing anti-HCV failed to prevent transmission of infection after exposure.

No clinical trials have been conducted to assess postexposure use of antiviral agents (e.g., interferon with or without ribavirin) to prevent HCV infection, and antivirals are not FDA-approved for this indication. Available data suggest that an established infection might need to be present before interferon can be an effective treatment. Kinetic studies suggest that the effect of interferon on chronic HCV infection occurs in two phases. During the first phase, interferon blocks the production or release of virus from infected cells. In the second phase, virus is eradicated from the infected cells (89); in this later phase, higher pretreatment alanine aminotransferase (ALT) levels correlate with an increasing decline in infected cells, and the rapidity of the decline correlates with viral clearance. In contrast, the effect of antiretrovirals when used for PEP after exposure to HIV is based on inhibition of HIV DNA synthesis early in the retroviral replicative cycle.

In the absence of PEP for HCV, recommendations for postexposure management are intended to achieve early identification of chronic disease and, if present, referral for evaluation of treatment options. However, a theoretical argument is that intervention with antivirals when HCV RNA first becomes detectable might prevent the development of chronic infection. Data from studies conducted outside the United States suggest that a short course of interferon started early in the course of acute hepatitis C is associated with a higher rate of resolved infection than that achieved when therapy is begun after chronic hepatitis C has been well established (90‚92). These studies used various treat-ment regimens and included persons with acute disease whose peak ALT levels were 500-1,000 IU/L at the time therapy was initiated (2.6-4 months after exposure).

No studies have evaluated the treatment of acute infection in persons with no evidence of liver disease (i.e., HCV RNA-positive <6 months duration with normal ALT levels); among patients with chronic HCV infection, the efficacy of antivirals has been demonstrated only among patients who also had evidence of chronic liver disease (i.e., abnormal ALT levels). In addition, treatment started early in the course of chronic HCV infection (i.e., 6 months after onset of infection) might be as effective as treatment started during acute infection (13). Because 15%‚25% of patients with acute HCV infection spontaneously resolve their infection (93), treatment of these patients during the acute phase could expose them unnecessarily to the discomfort and side effects of antiviral therapy.

Data upon which to base a recommendation for therapy of acute infection are insuf-ficient because a) no data exist regarding the effect of treating patients with acute infec-tion who have no evidence of disease, b) treatment started early in the course of chronic infection might be just as effective and would eliminate the need to treat persons who will spontaneously resolve their infection, and c) the appropriate regimen is unknown.