Viral hepatitis G

Introduction to hepatitis G virus As early as 1993, some people discovered that there were some new hepatitis viruses in addition to hepatitis A, B, C, D, and E. They were tentatively named as "non-A, B, C, D, E hepatitis." (HNA-E) virus." According to the different sequences, it is called GBV-A and GBV-B, and another new viral factor GBr-C was separated from the serum of HNA-E patients. At the 3rd International Hepatitis C and Related Virus Conference held in Australia in 1995, Kim and Bradley reported the discovery of a novel flavivirus-like RNA sequence with a higher genetic sequence than GBV-A/GBV-C. The homology was temporarily named as Hepatitis G Virus (HGV), and its official naming was finalized by the International Committee for Classification and Nomenclature of Viruses. basic knowledge Sickness ratio: 0.01%-0.02% Susceptible people: no specific population Mode of transmission: blood transmission mother-to-child transmission Complications: chronic hepatitis cirrhosis

The cause of hepatitis G virus

(1) Causes of the disease

HGV is a single-stranded positive-strand RNA virus with a full-length 9.4 kb gene and a large continuous, translatable single open reading frame encoding a multimeric precursor protein of more than 2870 amino acid residues. The 'end encoding structural protein, the 3' end encodes a non-structural protein, and the 5' non-coding region of the entire genome is the most conserved.

The circulating HGV may be covered by the host's lipoprotein and has sugar molecules on the surface, so the observed virus density is low. In vitro and in vivo experiments show that HGV is a hepatotropic virus that replicates in liver cells, so liver tissue and cells The genomic RNA and negative-strand RNA that can detect the virus are viral replication sites; only genomic RNA is detected in serum and lymphocytes, and negative-strand RNA is not detected, so no replication intermediate is considered, and HCV can be HgV infection is consistent with HCV in lymphocytes, but its infectivity is lower than HCV.

Computer sequence analysis showed that HGV has the highest homology with GBV-C. The nucleotide homology in the helicase region is 85.5%, and the amino acid homology is 100%. GBV-C is considered to be the West African of HGV. So far, the GBV-A, B sequence has not been amplified in human serum samples by RT-PCR.

(two) pathogenesis

Regarding the pathogenicity of HGV, there is still controversy. Some scholars believe that it is not pathogenic. Some HGV-positive people have hepatitis manifestations, which may be caused by another unknown hepatitis virus associated with HGV.

Hepatitis G virus prevention

The main source of HGV infection is blood transfusion and application of blood products. Therefore, screening blood and blood products is the main measure to prevent HGV infection. This requires clear, rapid and simple detection methods and reduces blood product contamination.

Hepatitis G complications Complications chronic hepatitis cirrhosis

Repeated episodes form chronic hepatitis and cirrhosis.

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Regarding the pathogenicity of HGV, there is still controversy. Some scholars believe that it is not pathogenic. Some HGV-positive people have hepatitis, which may be caused by another unknown hepatitis virus associated with HGV. The reasons are as follows: 1HGV genome has no core region, suggesting that it is a defective virus; 2 two chimpanzees have been followed up for 6 years and 3 months after being infected with HGV, and their serum HGV is persistently positive, indicating that persistent infection of HGV occurs. However, hepatitis has not appeared, serum alanine aminotransferase is normal, and liver tissue has no inflammatory changes. 3 Most patients with HGV have normal serum alanine aminotransferase; 4 patients with hepatitis B and hepatitis C have not been aggravated after infection with HGV. The serum alanine aminotransferase level was not significantly different from that of hepatitis B or hepatitis C virus alone, but some scholars believe that hepatitis G virus infection can cause acute and chronic hepatitis, and may also be related to acute severe hepatitis. The relevant content is summarized as follows.

HGV infected people may have 6 kinds of outcomes:

1 The virus was quickly cleared and the body was transiently infected.

2 The virus is chronically carried, but has no clinical symptoms and is in a normal carrying state.

3 Acute hepatitis appeared, but recovered quickly, the virus was cleared, and serum alanine aminotransferase (ALT) was reduced to normal levels.

4 delayed recovery, ALT has intermittent increase.

5 The condition is prolonged, recurrent, and chronic hepatitis is formed.

6 may cause fulminant hepatitis.

1. Acute infection of HGV It is reported that most acute infections of HGV are subclinical or jaundice-free, with only about 59% of HGV infections showing elevated transaminase, others may be "healthy" carriers and quiescent. The patient, Alter et al. found that the pathogen and clinical analysis of 268 patients with acute hepatitis found that in 47 patients with non-A to E hepatitis, 13% of the blood HGV RNA () had an average transaminase (ALT) level of 1689 U/L. The total bilirubin (TBil) level was 164 mol/L. Fukushima et al. compared acute hepatitis G and acute hepatitis A, B, and C. There was no significant difference in age, gender, AST, TBil, and clinical course. ALT is significantly different from hepatitis C. The average ALT of HGV infection is 1484.7 U/L, and the HCV infection is 639.6 U/L. It is also reported that the clinical symptoms of hepatitis G are mild, and the jaundice and ALT values are lower than those of hepatitis C.

HGV can cause post-transfusion hepatitis through blood transfusion. Feinman et al analyzed 20 cases of non-A-C transfusion hepatitis, 3 of which were positive for HGV RNA, and 3 cases were negative for serum HGV RNA before transfusion, and the time of transfusion was during blood transfusion. After 6 to 24 weeks, the clinical course, except 1 case had mild symptoms, the other 2 cases had no discomfort, and 3 cases had elevated ALT. After 5 years of follow-up, no case was converted to chronic, but 1 case lasted for 5 years. HGV RNA is positive.

2. Chronic infection of HGV The author believes that chronic hepatitis caused by HGV accounts for about 10% of all chronic hepatitis. In non-A, non-C, chronic hepatitis, HGV causes about 16%, but in patients with chronic hepatitis C. The infection rate of HGV was 18.75%. In a group of data, the average age of patients with chronic hepatitis G was higher, ranging from 53 to 68 years old. Most of these patients were diagnosed as cirrhosis. In the middle of the year, some scholars believe that the chronic hepatitis G rate may be lower than hepatitis C, it takes a long time to develop cirrhosis, but once cirrhosis occurs, the disease progresses very fast, but some scholars believe that although HGV Infection can occur in chronic infection or virus-carrying state, and the detection rate of HGV RNA in non-A-E hepatitis is high, but it cannot be considered that HGV infection can cause chronic hepatitis. Alter et al. have acute HGV RNA positive for 4 cases. Cases of hepatitis A to E were followed up for 1 to 9 years, and none of them developed chronic hepatitis, but 3 of them were persistently positive for HGV RNA. This result suggests that these patients are chronic HGV carriers, and their acute hepatitis symptoms are not related to HGV infection. In addition Other studies have found that the detection rate of HGV is not significantly different between ALT normal blood donors and ALT abnormal blood donors. This result also suggests that chronic infection of HGV does not cause liver damage or chronic hepatitis.

3. HGV and fulminant hepatitis on HGV caused by fulminant hepatitis, there is still controversy, some reports in the serum of non-A ~ E fulminant hepatitis patients detected HGV RNA, that HGV can cause fulminant hepatitis, patients clinically The performance is subacute, except for the rapid onset of coma in some patients, most patients from 14 to 19 days from symptom onset to coma, with persistent ALT fluctuations and increased serum bilirubin, fulminant hepatitis caused by HGV may Similar to the clinical trials of fulminant hepatitis caused by HCV, but some studies have proposed different arguments. They failed to detect HGV RNA in the serum of 9 patients with non-A to E fulminant hepatitis. The difference, on the one hand, is due to the small number of case samples studied, and on the other hand may be due to the variation of the HGV strain. In addition, the possibility that HGV infection does not cause fulminant hepatitis should also be considered.

4. Epidemiological and clinical studies of overlapping infection of HGV with HBV and HCV show that overlapping infection of HGV with HBV and HCV is more common, Nakatsuji et al., a group of cases for HGV RNA (RT-PCR) detection, chronic hepatitis B patients The positive rate was 4.9% (4/81); the positive rate of acute hepatitis B patients was 14.3% (3/21); the positive rate of chronic hepatitis C patients was 13.3% (14/105); that of acute hepatitis C patients was 13.2% (7/53), Linnen The positive rate of HGV in 72 cases of chronic hepatitis B in Europe was 9.72% (7/72); the positive rate of 96 cases of chronic hepatitis C was 18.75% (18/96). The above results indicated that the overlapping infection rate of HGV and HBV and HCV Higher, especially in patients with chronic hepatitis C, the overlapping infection rate is higher, and the co-propagation characteristics of the three viruses help explain why there is a high overlap rate.

Tancka et al analyzed 189 patients diagnosed with chronic hepatitis C by histological examination, 21 (11%) overlap HGV infection, and the infection-only group was younger than the overlap-infected group (mean age overlap infection group) The scores were 46.6±13.0 years old and 51.7±10.7 years old in the simple infection group. The gender, blood transfusion history, ALT level and liver biopsy were similar in the two groups, and the hepatitis C virus genotype and HGV RNA levels were basically the same. Therefore, HGV infection has no significant effect on the clinical and virological changes of HCV infection. Bralet et al observed 105 liver biopsies of patients with chronic hepatitis C, of which 17 (15%) were infected with HGV at the same time, using Knodell's scoring method and Metavir. Grading system, semi-quantitative examination of pathological histology of liver lesions, degree of hepatitis activity, fibrosis, lymph node aggregation at the portal site, steatosis, iron and iron deposition, etc., no significant difference between the individual and overlapping infection groups In HCV-infected patients, 19 cases (22%) had cirrhosis, and 2 cases (24%) had cirrhosis in double-infected patients. There was no significant difference between the two groups, which further explained the HGV infection to the liver. The impact of the disease is relatively small.

Examination of hepatitis G virus

The current laboratory diagnosis of HGV infection is mainly by using reverse transcription polymerase chain reaction (RT-PCR) to detect HGV RNA in serum and detecting anti-HGV antibodies in serum by enzyme-linked immunosorbent assay (EIA), human or animal. About 1 week after infection with hepatitis G virus, HGV RNA can be detected in serum, and anti-HGV antibody is generally positive after 3 weeks of infection. Therefore, RT-PCR can be used as an early diagnosis of hepatitis G virus infection. It is reported that the positive coincidence rate of EIA method and RT-PCR method is only 3%-18%, which is not suitable for laboratory diagnosis of HGV infection. However, the positive coincidence rate of anti-HGV EIA method and RT-PCR method developed by China recently can be Up to 60%, is expected to be used for screening for HGV infection.

Diagnosis and identification of hepatitis G virus

diagnosis

The current laboratory diagnosis of HGV infection is mainly by using reverse transcription polymerase chain reaction (RT-PCR) to detect HGV RNA in serum and detecting anti-HGV antibodies in serum by enzyme-linked immunosorbent assay (EIA), human or animal. About 1 week after infection with hepatitis G virus, HGV RNA can be detected in serum, and anti-HGV antibody is generally positive after 3 weeks of infection. Therefore, RT-PCR can be used as an early diagnosis of hepatitis G virus infection. It is reported that the positive coincidence rate of EIA method and RT-PCR method is only 3%-18%, which is not suitable for laboratory diagnosis of HGV infection. However, the positive coincidence rate of anti-HGV EIA method and RT-PCR method developed by China recently can be Up to 60%, is expected to be used for screening for HGV infection.

Tacke et al. reported that HGV coat protein E2 recombinant was used as an antigen in ELISA to detect anti-E2 in serum. It was found that anti-E2 in blood donors was 9% positive and HGV RNA positive was 25%. All anti-E2 positive patients were negative for HGV RNA. The positive rates of anti-E2 and HGV RNA in intravenous drug addicts were 41% and 38%, respectively, while HGV RNA increased with anti-E2 levels during drug injection. In parallel, 11 patients with hepatitis after transfusion had positive HGV RNA after transfusion, while anti-E2 was negative, but 4 of them had anti-E2 positive during follow-up, and 2 of 4 patients had negative HGV RNA. It is believed that the immune response to E2 is related to the disappearance of serum HGV RNA measured, so that specific E2 antibody can be an indicator for evaluating the recovery of HGV infection, but the protective effect of E2-specific antibodies against HGV infection, or in the clinical process. The role of this remains to be further explored.

Differential diagnosis

Must be differentiated from hepatitis B and hepatitis C.

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