An outbreak of enterically transmitted non‐A, non‐E viral hepatitis

Abstract

Patients with isolated serum transaminase elevations of unknown cause are common in China. An outbreak of such disease took place in a technicians' school during 1996. To define the epidemic and determine the etiology, a study was carried out, which included investigation of epidemiological, clinical and histological features. The symptoms of this disease were mild. The major clinical feature was transaminase elevation, and all serum markers of known hepatitis viruses were negative. Although the course of disease in most patients was self-limiting, in a few it was prolonged and relapsed. Histological findings were mild portal hepatitis or non-specific reactive hepatitis. The disease first appeared in 1994, and this outbreak occurred after October 1996. A total of 381 people were affected and the prevalence was as high as 60.7%. Casual contact and small-scale food transmission were considered to be risk factors for infection and the epidemic was under control 2 months later following the introduction of preventive measures for gastroenteric infection. Viral genomic fragments from the so-called transfusion-transmitted virus (TTV) were detected in acute-phase sera and stool samples collected 2 weeks before onset. Therefore, this disease outbreak might be another form of enterically transmitted viral hepatitis, not related to hepatitis A and E.

Prevalence and Phylogenetic Analysis of TT Virus DNA in Western India

“…In this connection it is important to note that TTV DNA has been detected in feces and bile samples and a possibility of fecal-oral transmission was suspected (16,23). A recent study attributing an outbreak of enterically transmitted non-A, non-E viral hepatitis to TTV is noteworthy (13). Among the rural populations of Nigeria, Gambia, Brazil, and Ecuador (20), TTV DNA positivity was found to be 7 to 74%.…”

Molecular Properties, Biology, and Clinical Implications of TT Virus, a Recently Identified Widespread Infectious Agent of Humans

“…Undoubtedly, the above observations rule out the notion that clinically evident liver disease is a frequent consequence of TTV infection. However, the evidence is not totally unequivocal, since data also exist that are compatible with the possibility that, in some cases, transient and mild abnormalities in liver enzyme levels are associated with TTV infection (33,34,56,61,65,68,81,88,110,126). Likewise, in several series of HCV patients, coinfection with TTV appeared to be associated with increased severity of biochemical and histological parameters of liver damage (15,22,48,56,172,175,191).…”

“…Additional observations corroborating this conclusion were as follows: (i) TTV DNA was detected in commercial human plasma, clotting-factor concentrates, and intramuscular immunoglobulin (Ig) preparations (133, On the other hand, from the very beginning it was also patent that TTV viremia rates in the general population were much too high to be explained solely in terms of apparent or inapparent blood-borne transmission. Feces of viremic individuals contain TTV (88,116,143,144,173), which is infectious in tissue culture (93) and nonhuman primates (87), suggesting the oral-fecal route as the most common mode of transmission. Undoubtedly, considering the high prevalence of virus carriers and the putative high resistance of TTV infectivity to physicochemical agents, even if TTV were shed in the stools only intermittently and/or at low titers, as existing data seem to indicate (116,144), the extent of TTV contamination in the human environment is likely to be remarkably high.…”

Clinicopathological study on TTV infection in hepatitis of unknown etiology

“…But some researchers did not think so. They think that TTV may cause epidemic outbreak of hepatitis of unknown etiology by fecal-to-mouth route [28] , and be responsible for some cases of non-A non-G hepatitis [47,48] . Some studies suggest that TTV can make other systems abnormal [49,50] and may be responsible for the development of hepatocellular carcinoma in patients with type C liver disease [51] .…”

“…The infection rate of TTV DNA varies largely in healthy population and patients with liver diseases, but generally, it is higher in patients than in healthy donors [7,[23][24][25][26] . The discovery of TTV once put a light on the etiological diagnoses of hepatitis cases of unknown etiology, unfortunately, the pathogenicity and clinical significance of TTV remain doubtful at this time [25,[27][28][29] . To clarify the infection status, replication place, pathogenicity and clinical significance of TTV among hepatitis cases, especially in patients of unknown etiology, we conducted the research to test TTV DNA comprehensively among large-sample cases of hepatitis.…”