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Isolated Presence of Antibody to Hepatitis B Core Antigen in Patients Coinfected With HIV
 
 
  Letter to the Editor
 
Guardado, Azucena Rodríguez*; Pérez, Mercedes Rodríguez†; Maradona, Jose A.*; Martínez, Ana†; Asensi, Victor*; Cartón, Jose A.*
 
*Infectious Diseases Unit, Hospital Central de Asturias, Oviedo, Spain
†Microbiology Unit, Hospital Central de Asturias, Oviedo, Spain
 
This article is dedicated to the memory of Ana Martinez.
 
To the Editor:
 
Antibody to hepatitis B core antigen (anti-HBc) is considered a sensitive and specific serum marker of hepatitis B virus (HBV) infection. Patients who have been infected with HBV and have recovered have antibody to hepatitis B surface antigen (anti-HBs), and those who are actively infected have hepatitis B surface antigen. In some patients, anti-HBc is the only marker of HBV infection. This finding could be due to false-positive results of reactivity testing, loss of anti-HBs with time or failure of patients to develop anti-HBs after HBV infection, occult chronic HBV infection with levels of hepatitis B surface antigen below the limits of detection, or a prolonged window phase of acute HBV infection.
 
Isolated reactivity to anti-HBc is observed relatively frequently in patients with HIV infection. We describe the characteristics of patients with isolated anti-HBc and HIV coinfection.
 
The presence of serological markers for HBV and hepatitis C virus (HCV) was investigated in 450 patients with infection by HIV. All patients had undergone testing for anti-HBc and anti-HBs. Patients who were positive for either antibody were evaluated for hepatitis B surface antigen, hepatitis B e antigen, and antibody to hepatitis B e antigen. Isolated anti-HBc was defined as positive results for anti-HBc with all the rest of the markers negative. The tests were done with commercially available kits (AXSYM System; Abbott Laboratories, Abbott Park, IL). Routine tests for determination of liver enzyme levels, CD4+ cell counts, and HIV load were performed simultaneous to serological studies.
 
Fifty-seven patients positive for anti-HBs and for anti-HBc (group 1) were compared with 47 patients with isolated anti-HBc (group 2). The X2 test was used for comparing qualitative determinations between the 2 groups, and the Student t test was used for quantitative variables.
 
The 2 groups did not differ statistically by sex (group 1, 80% men; group 2, 75% men) or age (group 1, 41 ± 7 years; group 2, 40 ± 5 years). There were no statistically significant differences in CD4+ cell count (group 1, 375 ± 257/mm3; group 2, 309 ± 280/mm3; P = 0.387) or HIV load (group 1, 155,579 ± 289,917 copies/mL; group 2, 243,641 ± 581,318 copies/mL; P = 0.2) between the 2 groups. Eighty-nine patients with isolated anti-HBc also had antibodies to HCV versus 47 patients with antibodies to HCV in group 2 (P = 0.0001). Multivariate analysis also showed a significant association between antibodies to HCV and the presence of isolated anti-HBc (P = 0.387). We did not observe statistically significant differences in liver enzyme levels (aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, and g- glutamyl transpeptidase) between the 2 groups.
 
The presence of isolated anti-HBc is observed relatively frequently in immunocompromised patients, intravenous drug users, and patients with HIV or HCV infection. Other studies have examined the influence of immunosuppression produced by HIV in the absence of production of or during the loss of anti-HBs. However, our results did not show a relation between CD4+ cell counts carried out simultaneous to serological tests and the presence of isolated anti-HBc. On the other hand, and like other studies, our results showed a greater statistical relation between the presence of antibodies to HCV and isolated anti-HBc. Some theories have attributed this fact to the possible interference in hepatitis B surface antigen synthesis by HCV infection, but the real cause is not clear.
 
In conclusion, the presence of isolated anti-HBc is frequent in patients with HIV infection, and it is statistically associated with HCV coinfection. However, its presence is not related to CD4+ cell count in these patients. The clinical significance of this association is not clear.
 
 
 
 
 
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