Surveillance and Control
• screening of blood and blood products with reliable kits of acceptable sensitivity and specificity to reduce the chances that the blood supply system may contain pathogens like HCV.
• vigorous implementation of universal precautions to prevent the spread of HCV.
Egypt has a very high prevalence of HCV and a high morbidity and mortality from chronic liver disease, cirrhosis, and hepatocellular carcinoma. Approximately 20% of Egyptian blood donors are anti-HCV positive. Egypt has higher rates of HCV than neighboring countries as well as other countries in the world with comparable socioeconomic conditions and hygienic standards for invasive medical, dental, or paramedical procedures. The strong homogeneity of HCV subtypes found in Egypt (mostly 4a) suggests an epidemic spread of HCV. Since a history of injection treatment has been implicated as a risk factor for HCV, a prime candidate to explain the high prevalence of HCV in Egypt is the past practice of parenteral therapy for schistosomiasis. The large reservoir of chronic HCV infection established in the course of these campaigns remains likely to be responsible for the high prevalence of HCV morbidity and may be largely responsible for the continued endemic transmission of HCV in Egypt today.49
In Italy the prevalence of anti-HCV is greater than 5% in some communities. In one region where the prevalence of anti-HCV was 12.6% overall, the rate among persons younger than 30 years of age was only 1.3% compared with 33.1% in those above 60. The demographic characteristics of this community were typical of many small towns in southern Italy. The use of glass syringes for medical treatment, a common practice before 1970 in Italy, or a history of dental therapy were found to be associated with anti-HCV positivity. A similar risk from immunizations in the 1950s using non-disposable syringes was reported from Japan.49
HCV Infection occurs throughout the world, and up until the introduction of anti-HCV screening tests for blood donors, introduced in 1990/1991 in Europe and the United States, it has represented the major cause of transfusion-associated hepatitis.39, 95
As many as 2 to 4 million persons may be chronically infected in the United States, 5 to 10 million in Europe, and about 12 million in India, and most do not know they are infected. About 150 000 new cases occur annually in the US and in Western Europe, and about 350 000 in Japan. Of these, about 25% are symptomatic, but 60 to 80% may progress to chronic liver disease, and 20% of these develop cirrhosis. About 5%-7% of patients may ultimately die of the consequences of the infection.3, 39, 41, 52, 74, 93, 96
WHO estimates that about 3% of the world’s population has been infected with HCV and that there are more than 170 million chronic carriers who are at risk of developing liver cirrhosis and/or liver cancer.5, 100, 101
Very high rates of HCV antibody reactivity (>70%) have been reported in injecting drug users and in haemophiliacs. Intermediate prevalences of 20 to 30% have been observed in patients receiving haemodialysis.96 The incidence is declining since transmission by blood products has been reduced to almost zero and universal precautions in medical settings are followed.5
Transfusion-associated cases occurred prior to donor screening. Now they are very rare where blood is screened with 2nd and 3rd generation EIAs, about 0.004% to 0.0004% per unit transfused.84, 94, 95
New HCV infections have decreased by over 80% since 1990 in the USA.56
The development of effective pre- and postexposure prophylaxis is complicated because of the genetic diversity of HCV.
No effective post-exposure prophylaxis (immune globulin, antiviral agents) is available for hepatitis C.56 Passive immune prophylaxis against HCV using immune globulin containing detectable levels of anti-HCV has not been convincingly documented and active immune prophylaxis is a goal for the future.94, 103 A preliminary study showed that administration of anti-HCV immune globulin to chimpanzees shortly after challenge delayed the onset of acute hepatitis.39
Mechanisms of the effect of interferon in treating patients with acute hepatitis C are still poorly understood. High SVR rates (83 to 100 percent) have been reported by small uncontrolled trials with interferon monotherapy. Accordingly, treatment of persons with acute hepatitis C is warranted, but the timing of therapy and the type of regimen to use remains to be determined from future trials. The preliminary evidence suggests that treatment with interferon in the early phase of infection43 or 2-4 months after infection leads to virus elimination in about 80% of cases.9, 34, 60, 72 The use of pegylated interferons does increase the sustained virological response (SVR) rate.
There is no vaccine against HCV.
There are major challenges to the future development of a hepatitis C vaccine. Primary infection of chimpanzees does not protect against subsequent challenge by either the identical viral strain or a heterologous strain. Protective or neutralizing antibodies have not been found.41, 52
An additional major obstacle to vaccine development is the extensive genetic variation between different strains and genotypes, and even the significant antigenic variation among virus quasispecies within individual patients.7, 41, 52, 97
Although an ideal vaccine should give immunity to infection, in the case of HCV, where acute HCV infection is a limited health problem and infection can only be assessed by PCR, a more realistic goal might be to find a vaccine that protects from chronic infection.7
In the absence of a vaccine, all precautions to prevent infection by other means must be taken.101