GNE-317 mg Human immunodeficiency virus type HIV is
Human immunodeficiency virus type 1 (HIV-1) is responsible for the GNE-317 mg pandemic; notification is compulsory in Brazilian blood banks since 1988. From 1980 to 2016, the Brazilian MH reported 882,810 HIV/AIDS cases, with 52.3% in the southeast region.
HIV/HCV co-infection has been associated with poorer outcomes of subsequent diseases.4, 8, 9 HIV/HTLV-1 co-infection induces rapid progression toward AIDS and death10, 11; HIV/HTLV-2 slows the progression toward AIDS.
Although HCV/HTLV-1/-2 co-infection has been associated with worse outcomes of HCV infection worldwide (higher HCV viremia, lower rate of sustained virological response to α-interferon treatment, increased risk of chronic liver disease, and cancer), this is not the case in Brazil. Indeed, in Brazil, HCV/HTLV-1 co-infection has been associated with spontaneous clearance of HCV, and less liver injury.9, 13, 14, 15, 16
Results Table 1 presents the characteristics of the study population (age and sex) as well as the results of HCV viral load for each group. No difference in relation to age was observed among the groups (p>0.05 in all analyses). Regarding gender, males comprised the majority of HCV/HIV co-infected patients (p=0.0002). Overall, the median HCV load was 5.29 log10 IU/mL, which was 0.34 log10 higher in men than in women. The same profile was observed in the HCV-monoinfected group, which presented a viral load of 5.23 log10 IU/mL, 0.31 log10 higher in men than in women. Viral load were 0.51 log10, 0.54 log10, and 1.43 log10 IU/mL higher in HCV/HIV-1-, HCV/HTLV-1-, and HCV/HIV/HTLV-1-co-infected individuals, respectively, compared to HCV-monoinfected counterparts. In contrast, an HCV load in HCV/HTLV-2-co-infected patients was 5.0 log10 IU/mL (0.23 log10 lower than in HCV-monoinfected patients); in HCV/HIV/HTLV-2-co-infected patients HCV load was 0.37 log10 IU/mL lower than in HCV/HIV-co-infected counterparts (Table 1). Of note, no patient had an undetectable serum viral load, and the current viral load was only determined in 33.3% of patients. Median viral load results were significantly different between males and females in the overall sample and in the HCV-monoinfected (p=0.0016 and p=0.0147, respectively) group. In addition, median viral load was lower in the HCV-monoinfected than HCV/HIV (p=0.0011), but the HCV/HIV group had lower viral load than the HCV/HIV/HTLV-1 (p=0.0433) group. Although it did not reach statistical significance (p=0.0721), median viral load in the HCV/HIV group had a trend to be higher than in the HCV/HTLV-2 group. Results of p>0.05 were obtained for all other analyses (data not shown). Fig. 2 shows these results, highlighting only the statistically significant associations.
Discussion The observed difference in the number of individuals with each type of viral infection or co-infection reflects the population characteristics of those visiting each service that sent samples to IAL for analysis. For instance, HCV/HIV co-infection was mostly present in HCV patients attending Infectious Diseases Services (STD/AIDS), whereas no HIV infection was detected in almost all samples from Gastroenterology and/or Hepatology Services of São Paulo (data not shown). Curiously, for the Gastroenterology Service of the city of São Paulo, HCV/HTLV-1/-2 co-infection was detected in 6.1% of patients, though none was HIV-infected. This is of concern, as HTLV serology is not routinely recommended in the clinical management of HCV-infected individuals in Brazil. Nonetheless, the Brazilian MH recommends performing at least one HTLV serology assessment during follow-up of HIV-1 infected individuals. Thus, we hypothesize that the patients attending STD/AIDS Centers are more likely to know their HTLV status than are those cared for at other services. Therefore, we suggest including HTLV serology in the battery of tests performed for HCV-infected patients in Brazil, regardless of their HIV-1 status.