Acute Symptomatic Infection with Recovery Any one of the hepatotropic viruses can cause symptomatic acute viral hepatitis, although this is uncommon for acute HCV infection. Whatever the agent, the disease is more or less the same and can be divided into four phases: (1) an incubation period, (2) a symptomatic preicteric phase, (3) a symptomatic icteric phase, and (4) convalescence. The incubation period for the different viruses is given in Table 18-6. Peak infectivity occurs during the last asymptomatic days of the incubation period and the early days of acute symptoms. The preicteric phase is marked by nonspecific, constitutional symptoms. Malaise is followed in a few days by general fatigability, nausea, and loss of appetite. Weight loss, low-grade fever, headaches, muscle and joint aches, and pains and diarrhea are inconstant symptoms. About 10% of patients with acute hepatitis, most often those with hepatitis B, develop a serum sickness-like syndrome. This consists of fever, rash, and arthralgias, attributable to circulating immune complexes. The true origin of all these symptoms is suggested by elevated serum aminotransferase levels. Physical examination reveals a mildly enlarged, tender liver. In some patients, the nonspecific symptoms are more severe, with higher fever, shaking chills, and headache, sometimes accompanied by right upper quadrant pain and tender liver enlargement. The icteric phase, if it appears, is caused mainly by conjugated hyperbilirubinemia. Icteric hepatitis is usual in adults (but not children) with acute HAV infection, but it is absent in about half the cases of HBV and in the majority of cases of HCV. Curiously, as jaundice appears and these patients enter the icteric phase, other symptoms begin to abate and the patient feels better. Although not the result of biliary obstruction, the jaundice is nevertheless caused predominantly by conjugated hyperbilirubinemia and hence is accompanied by dark-colored urine related to the presence of conjugated bilirubin. The stools may become lighter owing to cholestasis. Retention of bile acids can cause distressing pruritus. The liver may be mildly enlarged and moderately tender to percussion. Laboratory findings include prolonged prothrombin time and hyperglobulinemia; the serum alkaline phosphatase is usually only mildly elevated. In a few weeks to perhaps several months, the jaundice and most of the other systemic symptoms clear as convalescence begins. Recovery is heralded by the generation of strong T cell responses against viral antigens expressed on infected liver cells.