Hepatitis C doesn't affect cognitive function of women, but some evidence HIV does

Infection with hepatitis C does not affect the cognitive performance of women with or at risk of HIV, according to data from the Women’s Interagency HIV Study (WIHS) published in the online edition of the Journal of Acquired Immune Deficiency Syndromes.

“We were unable to show a significant association between the presence of HCV [hepatitis C virus]…and performance on our cognitive battery nor that there is an interaction between HIV and HCV in their effect on cognitive function,” write  the authors.

However, their was some evidence that infection with HIV had an impact on cognition.

A number of earlier studies have suggested that hepatitis C-infected individuals have an increased risk of neurocognitive impairments. Moreover, replicating virus has been found in the brains of patients with the infection. It has also been suggested that co-infection with HIV and hepatitis C could have a worse impact on cognitive function than either virus alone.

Women have been unrepresented in research exploring the impact of hepatitis C on cognition. Therefore, investigators from the WIHS designed a study involving 1338. Just under a fifth (18%) had detectable hepatitis C virus and 67% were infected with HIV.

“To our knowledge this cohort for our study is over twice as large as any previously reported study of the effects of HCV and HIV on cognition,” note the investigators.

The patients were divided into six groups:

Negative for both HIV and hepatitis C RNA (392 individuals).

HIV-negative/hepatitis C RNA-positive (42 individuals).

HIV-positive/hepatitis C RNA-negative (480 individuals).

AIDS/hepatitis C RNA-negative (241 individuals).

AIDS/hepatitis C RNA-positive (88 individuals)

The patients had a battery of four tests to assess their cognitive function. The results were controlled for age, ethnicity, depression, liver disease status and current or past drug and alcohol abuse, all of which have been shown to affect cognitive function.

There were significant differences between the patients according to their hepatitis C and/or HIV-infection status.

Individuals infected with hepatitis C were a significant nine years older than women who did not have hepatitis C (p < 0.001). Rates of injecting drug use were also significantly higher among the women with hepatitis C (85% vs. 12%), and hepatitis C-infected women were also significantly more likely to report recent use of cocaine (p < 0.001).

As expected, liver function was significantly poorer in those infected with hepatitis C, and the women with an AIDS diagnosis had lower CD4 cell counts than other individuals (p = 0.001).

After controlling for potential confounders, the investigators failed to find any association between hepatitis C viraemia and cognitive performance.

In their first set of analysis, they established a significant connection between poorer liver function and poorer cognitive function (p < 0.001). However, this relationship disappeared after controlling for factors such as age, ethnicity, depression and general mental health.

Nevertheless, infection with HIV was associated with impaired speed of information processing and perceptual motor ability (p < 0.001).

The investigators do not regard their findings as definitive: “The question of whether HCV has a direct effect on cognition will require future studies with a complete neuropsychological batter, a large control group and a large group of HCV-mono-infected subjects.” They also believe that such studies would need “a cohort that includes both men and women.”

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Hepatitis B genotype B associated with poorer liver-related outcomes in Taiwanese patients co-infected with HIV and hepatitis B

Liver-related outcomes are poorer in HIV-positive patients who are co-infected with hepatitis B virus genotype B compared to co-infected patients with hepatitis B genotype C, Taiwanese investigators report in the online edition of Clinical Infectious Diseases.

The prospective, observational study involved individuals who commenced antiretroviral therapy containing 3TC (lamivudine, Epivir, also in the combination pill Combivir), a drug which has activity against both viruses. The patients were recruited between 1997 and 2008, and followed until 2010.

“Patients with [hepatitis B virus] genotype B co-infection were at higher risk of developing hepatitis flares, liver disease-related deaths, HBeAg seroconversion, and lamivudine resistance mutations than those with genotype C coinfection,” write the authors. Genotype did not affect HIV-related outcomes.

HIV and hepatitis B share transmission modes. Therefore, large numbers of patients are co-infected with these viruses. There are eight hepatitis B genotypes (A – H). The distribution of genotypes varies according to geographical region, and genotypes B and C predominate in Asia.

Little is known about the differential impact of these two genotypes on liver-related outcomes in patients co-infected with HIV and hepatitis B.

Therefore, investigators in Taiwan recruited 145 co-infected patients starting antiretroviral therapy to a study analysing the clinical, immunological and virological outcomes of patients according to hepatitis B genotype.

The hepatitis B-related outcomes included the risk of hepatitis flares, liver disease-related death, hepatitis B e antigen (HBeAg) seroconversion, and the development of strains of hepatitis B with resistance to 3TC. Changes in CD4 cell count and HIV viral load were also compared according to genotype.

A total of 96 patients were co-infected with genotype B and 49 with genotype C were recruited. There were no significant baseline differences between the patients.

However, they had severe immune suppression at the time they started HIV treatment, and their median CD4 cell count was just 117 cells/mm3. Median baseline HIV viral load was approximately 125,000 copies/ml. Median hepatitis B viral load at the start of the study was 63,000 copies/ml.

Patients were treated with 3TC-containing antiretroviral therapy for a median of 2.8 years. During this time, none of the patients received any other antiretroviral drugs with activity against hepatitis B.

Compared to patients with genotype C, those with genotype B co-infection were significantly more likely to experience hepatitis flares (44% vs. 27%, p = 0.04), die of liver-related causes (9% vs. 0%, p = 0.03), have HBeAg seroconversion (62% vs. 25%, p = 0.03), and developed strains of hepatitis B with resistant to 3TC (31% vs. 12%, p < 0.001).

Analysis that controlled for potentially confounding factors confirmed the relationship between genotype B co-infection and a number of liver-related outcomes.

Compared to individuals with genotype C, those with genotype B had a higher risk of hepatitis flares (AHR = 4.13; 95% CI, 2.87-5.39; p = 0.01) and were also more likely to develop 3TC-resistant hepatitis B (AHR = 8.67; 95% CI, 6.37-10.98, p = 0.001).

However, there was no significant difference in mortality risk between the genotypes. Nor did HIV-related outcomes differ between the two groups of patients, who had similar falls in viral load and increases in CD4 cell count.

“Hepatitis B genotype B is the most predominant genotype in hepatitis B virus and HIV-co-infected Taiwanese patients,” conclude the investigators. “Patients with genotype B co-infection are more likely to experience acute exacerbations of hepatitis, HBeAg seroconversion, lamivudine resistance, and liver disease-related death than those with genotype C coinfection when they receive [HIV therapy] containing lamivudine as the only active agent against hepatitis B virus.”

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