Viruses which affect the liver

In this study, NGS revealed the importance of the last generation of hepatotropic viruses rather than a new generation of viruses. Decreasing costs of NGS platforms may make unbiased sequence detection of pathogens in blood increasingly attractive. NGS could play an important diagnostic role in the future; however, additional studies are needed to compare NGS with existing approaches where the performance characteristics of NGS are compared to those of polymerase chain reaction PCR and serology for large numbers of patients with known viral hepatitis.

The study by Somaseker et al does not inform how metagenomic NGS performs for all cases of ALF including those caused by known viruses vs mostly indeterminate in their study where sensitivity, specificity, and positive and negative predictive values are assessed.

Furthermore, viral nucleic acid detection in blood may fail diagnostically when pathology is driven more by immune control of virus rather than viral replication and resulting cytopathic effect, such as seen with hepatitis B virus; in this scenario, serology may be more useful than nucleic acid—based detection of virus. It is possible that some common viruses such as parvovirus B19 or CMV are etiological agents of ALF in adults, but we will need more convincing evidence than that provided by detection of virus in blood.

Future studies should strive to obtain liver tissue via explanted livers at the time of liver transplantation, or via transjugular catheter biopsy of the liver in those not undergoing transplantation. Demonstration of viral infection in the liver using quantitative PCR, immunohistochemistry, or in situ hybridization methods will be critical to convince skeptics that these common viruses produce an uncommon pathological event leading to ALF.

Given the common finding of human herpesvirus detection in blood of critically ill patients [ 14 ], it is more likely that detection of these viruses in the blood of patients with ALF represents the presence of bystanders and not instigators of pathology. It is possible that some patients in the Somaseker et al study had viral infections that were not detected by metagenomic NGS because blood was sampled after the period of viremia, or because the DNase treatment destroyed low levels of viral DNA after freeze-thaw damage to viral particles.

However, in aggregate this well-executed study suggests that novel viruses are not a common cause of ALF. These data should encourage clinicians to use our current diagnostic tools such as PCR to rule out treatable infectious causes of ALF such as herpes simplex virus and hepatitis B virus. The value of NGS as a replacement for current viral diagnostics remains to be proven.

Potential conflicts of interest. Author certifies no potential conflicts of interest. Conflicts that the editors consider relevant to the content of the manuscript have been disclosed. Control of hepatocellular carcinoma through hepatitis B vaccination in areas of high endemicity: perspectives for global liver cancer prevention.

Cancer Lett ; : 15 — Google Scholar. Bernal W , Wendon J. Acute liver failure. N Engl J Med ; : — 1. Lessons from look-back in acute liver failure? A single centre experience of patients. J Hepatol ; 59 : 74 — Etiology and outcome of acute liver failure: experience from a liver transplantation centre in Montreal.

Can J Gastroenterol ; 16 : — 6. Surveillance for acute viral hepatitis—United States, Hepatitis E virus infection as a possible cause of acute liver failure in Europe. Clin Gastroenterol Hepatol ; 13 : — Science ; : — It affects liver together with heart, kidneys and spleen causing jaundice hemorrhages and marked albuminuria.

Diagnosis is made by virus isolation and serology. There is an effective vaccine, 17D which confers a long-standing immunity 35 years. It is safe for adults but should not be used in children under 6 months because it may cause encephalitis.

The liver is involved together with conjunctiva, pharynx, lymph nodes, skin. There is marked hepatocyte damage in the liver consisting in eosinophilic necrosis of individual cells but jaundice is rare.

The first infection occurred in among laboratory personnel in Marburg, Germany and in Yugoslavia with 7 deaths. Fever, rash, diarrhea, hemorrhages are the clinical manifestations in man. The liver suffers a necroinflammatory picture suggestive of a viral disease. No other infections have been reported lately. It exploded in East Africa: 70 cases with 33 deaths in Nzara, Sudan; 76 cases with 41 deaths in Maridi hospital; cases in Zaire with deaths.

The virus, like Marburg virus is an RNA particle that has been named Ebola after a small river in Zaire and belongs to the family of Filoviridae consisting of filamentous and branched forms. Try out PMC Labs and tell us what you think. Learn More. The liver is involved in infections by hepatotropic viruses that replicate in the liver and for which the liver is the main target. These include hepatitis A, hepatitis B, hepatitis C, and hepatitis E viruses.

In all of these infections, hepatitis and liver damage arise as a consequence of the immune response to virus within the liver. Examples of this phenomenon include the herpes viruses Epstein-Barr virus, cytomegalovirus [CMV], and herpes simplex virus , parvovirus, adenovirus, 2 and severe acute respiratory syndrome SARS -associated coronavirus.

In most of these infections, hepatitis is thought to be a consequence of an immune response to viral antigens with a close topographic association between the presence of viral antigens and the associated inflammatory infiltrates in the liver. Loss of immune control may be responsible for the development of hepatitis in CMV hepatitis 4 and other opportunistic viral infections such as adenovirus. They describe the involvement of the liver during pulmonary infection with influenza virus and demonstrate that hepatitis can occur even in the absence of detectable virus in the liver.

These observations are of great importance for understanding the involvement of the liver in systemic infections and elucidate some of the clinical syndromes of liver inflammation that cannot be easily explained by invoking antigen-specific T-cell responses in the liver.

It is known that severe influenza infection can be associated with abnormalities in liver biochemistry that resolve after successful clearance of the virus, 7 but the current study is the first to look systematically for liver involvement in volunteers infected with influenza virus. Interestingly, the rise in liver enzymes occurred after pyrexia had settled, suggesting that it was not driven by the initial viral replication and consequent activation of innate immune responses.

As the authors point out, the occurrence of hepatitis in influenza is intriguing because most strains of the virus only infect the epithelial cells of the respiratory tract, and viral antigens should not therefore be present in the liver.

To investigate the immunopathology and kinetics of the hepatitis in more detail, they used a murine model in which both primary and secondary immune responses to influenza infection could be studied. Intriguingly, the hepatitis was markedly less severe in the absence of Kupffer cells, the resident macrophages of the liver. The study raises several questions. First, how and why are activated T cells recruited to the liver in the absence of antigen? Previous studies have shown that activated T cells are retained in the liver in an antigen-independent manner as a consequence of interactions in the hepatic sinusoids between activated integrins on the T cell and constitutively expressed integrin ligands on sinusoidal endothelium.

This contrasts with the diffuse infiltrate of portal tracts and lobules seen when lymphocytes are responding to hepatic antigen in livers infected with hepatotropic viruses.

Second, after being trapped in the sinusoids, how do effector T cells mediate liver damage in the absence of their cognate antigen? One mechanism could be local ischemic necrosis precipitated by trapping of lymphocytes in the sinusoids and the consequent disturbance in blood flow. Your health is more than just about your liver. If you want other information about your health, see our Commonwealth partner HealthDirect.

Hepatitis NSW acknowledges the traditional custodians of the land on which we are based, the Gadigal people. We pay our respect to their Elders, both past and present and extend that respect to other Aboriginal and Torres Strait Islander peoples. What Causes Liver Damage and Disease? Types of viral infections that damage the liver The liver can be damaged by a few different viral infections.

Hepatitis A Hepatitis A is a liver infection caused by the hepatitis A virus. Hepatitis B Hepatitis B is the most common liver infection in the world, caused by the hepatitis B virus. Hepatitis C Hepatitis C is an easily cured liver infection , caused by the hepatitis C virus. Alcohol related hepatitis Alcohol-related hepatitis is a very common form of liver disease in Australia.

Click here for more information about alcohol related hepatitis … Non-alcoholic fatty liver disease Non-alcoholic fatty liver disease NAFLD happens when fat begins to build up in your liver. Click here for more information about autoimmune hepatitis … Lifestyle, Diet and Liver Damage Lifestyle and diet play a big role in your liver health. Contact the Hepatitis Infoline for more information Have questions about the causes of liver damage and disease?