HIV and Hepatitis.com Coverage of the
15th Conference on Retroviruses and Opportunistic Infections (CROI 2008)
 February 3 - 6, 2008, Boston, MA
The material posted on HIV and Hepatitis.com about CROI 2008 is not approved
by nor is it a part of CROI 2008.
CROI 2008

Hepatitis B Coinfection Does Not Impact HIV Suppression or CD4 Cell Recovery on HAART

By Liz Highleyman

HBV VIRUS
Hepatitis B
is a serious disease caused by a virus that attacks the liver.

Due to similar routes of infection, many HIV positive people either have evidence of past hepatitis B virus (HBV) infection or chronic HIV-HBV coinfection. However, HIV-HBV coinfection has been less extensively studied than HIV-HCV coinfection.

Three studies presented at the 15th Conference on Retroviruses and Opportunistic Infections this month in Boston looked at the impact of HBV coinfection on virological and immunological response to HAART.

MACS Cohort

Researchers with the Multicenter AIDS Cohort Study (MACS) looked at HIV suppression, CD4 cell recovery, and rates of death among 822 participants who initiated antiretroviral therapy; 354 were never infected with HBV (HBcAb negative), 359 had evidence of past cleared HBV infection (HBsAb and HBcAb positive), 45 had chronic hepatitis B (HBsAg positive at 2 visits), and 64 had possible occult HBV infection (HBcAb positive only).

Results

Of the 64 HBcAb positive only participants, 7 had detectable HBV DNA.

The risk of AIDS-related death was not increased in any of the 4 HBV infection status groups.

However, rates of non-AIDS-related death were higher in the chronic hepatitis B and HBcAb positive only groups compared with never-infected subjects.

Of 6 deaths among HBsAg positive chronic hepatitis B patients, 4 were liver-related.

By contrast, none of the 4 deaths in the HBcAb positive only group were liver-related.

In adjusted models, there was no observed difference in HIV RNA suppression or CD4 cell recovery across the 4 HBV infection categories.

"In this well-characterized, prospectively followed cohort receiving long-term antiretroviral therapy, past or present infection with HBV did not alter the long-term immunological response to antiretroviral therapy as measured by HIV RNA suppression or CD4 response," the researchers wrote.

HIV-HBV in South Africa

In parts of Africa and Asia, chronic HBV coinfection is estimated to occur in 10%-20% of HIV positive individuals. Researchers in South Africa evaluated the effect of HBV infection on HIV virological response, CD4 cell recovery, hepatotoxicity, and death among a cohort of patients receiving anti-HIV treatment.

They prospectively studied 537 patients in a multi-site workplace cohort during the first 72 weeks on antiretroviral therapy consisting of AZT (zidovudine, Retrovir), 3TC (lamivudine, Epivir), and efavirenz (Sustiva). Subjects were stratified as hepatitis B surface antigen (HBsAg) positive or negative and with high or low HBV DNA (above or below 104 copies/mL).

Results

431 patients (80.2%) were HBsAg negative.

60 (11.2%) had low HBV DNA and 46 (8.6%) had high HBV DNA.

All groups had similar HIV viral load suppression and CD4 cell gains during 72 weeks on HAART.

Baseline liver enzyme (ALT and AST) levels were higher in the high HBV DNA group compared with the other 2 groups

Hepatotoxicity risk was similar between the HBsAg negative and low HBV DNA groups, but higher for the high HBV DNA group.

Based on these findings, the investigators concluded, "We have shown that HBV status does not affect HIV RNA suppression or CD4 response during the first 72 weeks of HAART in an African setting."

But, they added, "this is the first study to demonstrate that risk of HBV-associated hepatotoxicity is associated with baseline HBV DNA level."

HIV-HBV in South Africa

Finally, another team of researchers tested the hypothesis that high HBV DNA levels would influence pre-HAART HIV disease stage and antiretroviral hepatotoxicity, but would not affect antiretroviral response.

This study included 1305 HIV monoinfected and 264 HIV-HBV coinfected patients without hepatitis C who started HAART in Nigeria. Here, too, patients were stratified by HBsAg status and high or low HBV DNA (above or below (20,000 IU/ml). Comparisons were made at baseline and after months 3 and 6 on antiretroviral therapy.

Results

The median baseline CD4 count was lower in the HIV-HBV coinfected group with high HBV DNA compared with the HIV monoinfected and coinfected low HBV DNA groups (89, 130, and 129 cells/mm3, respectively).

Stratification by HBeAg status revealed that the median baseline CD4 count in HBeAg negative low HBV DNA patients was similar to that of the HIV monoinfected group (129 and 130 cells/mm3, respectively); all other groups had lower median baseline counts.

The median baseline HIV RNA level was similar between the HIV-HBV coinfected groups with high and low HBV DNA (89,882 and 96,895 copies/mL, respectively), which was significantly higher than that of the HIV monoinfected group (55,708 copies/mL).

After 6 months on antiretroviral therapy, neither HBV DNA level nor HBeAg status altered the percentage of patients who suppressed HIV RNA below 400 copies/mL.

CD4 counts increased in all groups at 6 months, but those with high HBV

DNA had lower median CD4 counts (216 vs 229 cells/mm3 for low HBV DNA and 240 cells/mm3 for HIV only); HBeAg status did not alter this relationship.

The high HBV DNA group had significantly higher median baseline ALT and the greatest cumulative rate of hepatotoxicity by month 6 (12% vs 4%-5%).

"In this HIV-HBV coinfected Nigerian cohort, high HBV DNA levels were associated with lower baseline CD4 counts and increased risk for hepatotoxicity on antiretroviral therapy," the researchers concluded. "High HBV DNA levels did not clearly impair immunological and virological responses with 6 months of antiretroviral therapy, but CD4 counts remained lower in those with high HBV DNA."

02/26/08

References

C Hoffmann, E Seaberg, K D'Acunto, and others. Death, HIV Suppression, and CD4 Recovery among HIV/HBV-co-infected Men Receiving ART: MACS. 15th Conference on Retroviruses and Opportunistic Infections (CROI 2008). Boston, MA. February 3-6, 2008. Abstract 1029.

C Hoffmann, S Charalambous, D Martin, and others. Chronic HBV/HIV Co-infection and HIV Suppression, CD4 Recovery, Mortality, and Hepatotoxicity in an African ART Cohort. CROI 2008. Abstract 1030.

J Idoko, S Meloni, M Muazu, and others. Effect of HBV DNA Levels on HIV Infection and Response to ART in a HIV/HBV-co-infected Nigerian Cohort. CROI 2008. Abstract 1031.


 
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