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Coinfection

DDW 2014: Outcomes in HBV/HCV Coinfected People Depend on Which Virus Dominates

Among HBV/HCV coinfected people, about half have dominant hepatitis B virus while half have dominant hepatitis C, and those with active HBV replication are at higher risk of liver-related complications and death, according to study findings presented at Digestive Disease Week this month in Chicago.

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CROI 2010: HIV/HBV and HIV/HCV Coinfected People with Impaired Liver Function and Inflammation Have Higher Risk of Non-AIDS Death

HIV positive study participants with hepatitis B virus (HBV) or hepatitis C virus (HCV) coinfection who had higher blood levels of biomarkers associated with impaired liver function and inflammation were more likely to die of non-AIDS-related causes, researchers with the SMART treatment interruption trial reported last month at the 17th Conference on Retroviruses and Opportunistic Infections (CROI 2010) in San Francisco.

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ICAAC 2008: Another Study Confirms Hepatitis B Virus Suppresses Hepatitis C Virus Replication in HBV-HCV Coinfected Individuals

Due to overlapping transmission routes, many people are dually infected with both hepatitis B virus (HBV) and hepatitis C virus (HCV).

In a poster presentation this week at the 48th International Conference on Antimicrobial Agents and Chemotherapy (ICAAC) in Washington, DC, Italian researchers presented data confirming prior research showing that the presence of HBV interferes with HCV replication.

The investigators performed long-term clinical and virological follow-up of 29 chronic hepatitis C patients with HBV superinfection and 29 HCV negative individuals with acute hepatitis B. Patients in the 2 groups were matched for age (+/- 5 years), sex, and HBV risk factors.

Results

• At the first observation, HBV-HCV coinfected patients and HBV monoinfected individuals had similar HBV DNA viral load (mean 7.1 vs 1.6 x 108) and a similar trend towards becoming HBV negative (HBV clearance).

• Severe acute hepatitis B was more frequent in the HBV-HCV coinfected group than in the HBV monoinfected group (34.5% vs 6.9%; P < 0.05).

• Of the 28 patients in the HBV-HCV superinfection group who were still alive at the end of acute illness (1 died of sub-acute progressive hepatitis), 24 (85.7%) were followed for 2-6 years (median 5 years):

• 21 of these 24 patients became hepatitis B surface antigen (HBsAg) negative (87.5%);

• 2 progressed to HBsAg positive chronic hepatitis (8.3%);

• 1 underwent liver transplantation (4.1%).

• Data on HCV RNA levels before the development of acute hepatitis B and every 12 months thereafter were available for 19 patients:

• All became HCV RNA negative during the acute phase of hepatitis B (100%);

• 16 patients still had undetectable plasma HCV RNA after 1 year (84.2%);

• 9 still had undetectable HCV RNA after 2 years (47.4%);

• 6 still had undetectable HCV viral load after 3-6 years (31.6%).

• The 6 patients who remained persistently HCV RNA negative during follow-up were compared with the 13 who experienced reactivation of HCV replication:

• During the acute phase of hepatitis B, there were no observed differences in HBV viral load (P = 0.4);

• Serum ALT values, however, were higher in the persistently HCV negative subgroup (mean 5291 vs 2208; P < 0.01).

Based on these findings, the researchers concluded, "HBV superinfection in HCV chronic carriers was associated with a strong inhibition [of] HCV replication," especially in 6 patients with marked hepatonecrosis who fully cleared chronic HCV infection.

Second Univ. of Naples, Naples, Italy; A.O. San Sebastiano e Sant'Anna Caserta, Caserta, Italy.

10/31/08

Reference

E Sagnelli, N Coppola, M Pisaturo, and others. HBV Superinfection in Chronic HCV Carriers: Clinical and Virological Long-Term Follow-Up Study. 48th International Conference on Antimicrobial Agents and Chemotherapy (ICAAC 2008). Washington, DC. October 25-28, 2008. Abstract V-1628.

 

Adefovir plus Hepatitis C Therapy May Prevent HBV Reactivation in HBV-HCV Coinfected Patients

Due to the similar transmission routes, many people are dually infected with both hepatitis B virus (HBV) and hepatitis C virus (HCV). While the interaction between these 2 viruses is not fully understood, studies have shown that HBV seems to inhibit HCV replication and vice versa. As such, there is a risk that successful treatment of one virus could potentially lead to worsening or reactivation of the other.

In a brief report in the December 2008 European Journal of Gastroenterology and Hepatology, French researchers described a case in which an HBV-HCV coinfected patient was simultaneously treated with both interferon-based therapy for chronic hepatitis C and the FDA-approved anti-HBV drug adefovir (Hepsera).

The authors observed that HBV reactivation as the result of HCV eradication was prevented by treating both viral infections together.

This finding, they concluded, "raises the question as to whether preemptive HBV treatment should be prescribed along with HCV treatment to prevent HBV from being [reactivated] after HCV eradication in coinfected HBV-HCV patients."

1/16/09

Reference

C Renou, JF Cadranel, A Pariente, and others. Adefovir combined with hepatitis C virus treatment may prevent hepatitis B reactivation after hepatitis C virus eradication in hepatitis B and C virus carriers. European Journal of Gastroenterology and Hepatology 20(12):1235-1237. December 2008. (Abstract).

 

Liver Enzyme Flares and Occult HBV Infection in Patients with Untreated Chronic Hepatitis C

Occult hepatitis B virus (HBV) infection has been reported in numerous clinical settings, but it remains unclear whether occult HBV contributes to liver damage. Given that typical chronic HBV infection is often characterized by periodic flares in viral replication and liver inflammation, investigators from Johns Hopkins School of Medicine hypothesized that occult HBV might also be associated with flares in viral replication that are associated with increased liver enzyme levels.

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