Acute HCV infection refers to the 6-month period after infection acquisition, although definitions vary117 and the distinction between acute and early chronic infection is somewhat arbitrary. In Australia, modelling suggests that the incidence of HCV infection peaked at 14 000 new infections in 1999 and declined to 8500–9000 new infections in 2013.[1,3] There is evidence of further declines in the incidence of HCV infection since the unrestricted availability of DAA therapy in 2016. In certain subpopulations, including HIV-positive MSM, incidence has declined dramatically.[118-124]
While in some cases acute HCV infection may develop after discrete exposure (eg, a needle-stick injury in a health care worker), detection of acute HCV infection is often hampered by its asymptomatic or non-specific presentation, lack of specific diagnostic tests and the inherent difficulties in identifying and following individuals at highest risk of transmitting and acquiring HCV, including PWID. Another high-risk group for HCV transmission is HIV-positive MSM, in whom sexual or permucosal transmission has become increasingly common.[97,125,126] Risk factors for sexual transmission include, but are not limited to, traumatic sexual practices, recreational non-injecting drug use, group sex and the presence of a coexistent sexually transmitted infection.
Acute HCV infection is characterised by the appearance of HCV RNA in blood within 2–14 days of exposure, elevation of liver-associated enzyme levels (particularly ALT), and development of HCV antibodies within 30–60 days of exposure. Up to 80% of acute HCV infections are asymptomatic, making detection and estimation of duration of infection difficult if seroconversion cannot be documented.
Clinical features suggestive of acute infection include significant elevation of ALT level or an acute illness manifest by jaundice. However, only 15%–30% of those infected develop a symptomatic illness, and elevation of ALT level is non-specific. Acute infection should be suspected if the clinical signs and symptoms are compatible with acute hepatitis C — such as serum ALT level > 10 x ULN and jaundice in the absence of a history of chronic liver disease or other causes of acute hepatitis, and/or if a likely recent source of transmission is identifiable.
The preferred criteria for diagnosis of acute HCV infection are:
i) positive anti-HCV IgG and a documented negative anti-HCV IgG in the previous 12 months; or
ii) positive serum HCV RNA test and a documented negative serum HCV RNA test and negative anti-HCV IgG in the previous 12 months.
Alternative, less stringent criteria are the presence of positive serum HCV RNA regardless of anti-HCV IgG and with:
i) an acute rise in ALT level > 10 x ULN; or
ii) an acute rise in ALT level > 5 x ULN, with documented normal ALT level within the past 12 months; or
iii) in individuals with a previously high ALT level, an acute rise to 3.5 times the baseline ALT level; and in the absence of serological evidence of HAV or HBV infection or other causes of acute hepatitis.
Documentation of seroconversion is difficult in the absence of routine serological testing, but monitoring of at-risk populations, including PWID, and HIV-positive MSM, may be beneficial. There is no single definitive laboratory test to distinguish acute from chronic HCV infection.