The prevalence of HPgV-1 among blood donors was 12,4%, which is consistent and not significantly different from the expected prevalence in developing countries (up to 20%) [4, 31]. The prevalence calculated in this study was 2,8% higher than reported Slavov et al.  in a study among blood donors from the city of Macapá (northern Brazil). Previous studies have shown that the prevalence of HPgV among blood donors in most regions of Brazil varies from 5–10% [14, 33–36], although Da Mota et al.  have found a high prevalence of 21.7% in the southernmost region of Brazil.
A significant association was observed between the presence of HPgV and age, gender, and years of education by Miranda et al. . In our findings, the highest prevalence of HPgV occurred among subjects between 18 and 30 years of age (16.5%), males (15.8%), and brown individuals (13.2%). It is important to highlight that the epidemiological profile of the donors was similar to that observed in the epidemiology of HIV/AIDS in Brazil, wherein the majority of the infected individuals were male and young subjects (15 to 39 years) with up to 11 years of age (completed high school) . Another issue to consider is that sexual activity is more evident among young people so this population has shown a greater risk to be infected with HPgV, as suggested Da Mota et al.  and Miao et al .
The prevalence of HPgV among the individuals diagnosed with HIV-1 in this study was 9,7% higher than that reported by Miranda et al. . The high prevalence of HPgV among HIV-1 individuals has been reported in several studies in Brazil and the world [40–42]. The association between the presence of HPgV and HIV is owing to the fact that HPgV likely acts as a protective factor for the development of HIV [40, 43, 44].
HIV-1 infected people have reduced mortality when co-infected with HPgV, nonetheless the mechanism by which HPgV mediates this protective effect remains unknown [45, 46]. Nevertheless, the present study showed no evidence of viral load value that corroborated with the protective effect of HPgV in the evolution of HIV, instead, HIV-1 viral load in the coinfected group (HIV-1 + HPgV positive) was 0.72 Log10 (p = 0,002) higher than in a monoinfected group (HIV-1 positive). One interpretation of this finding is that the increase in T cells during the expansion phase of viral infection leads to an increase in both viral loads [47, 48]. Another consideration is that all individuals in our sample were newly diagnosed with HIV during the acute phase, suggesting that HPgV does not exert a protective effect on the pathogenesis of HIV during the acute phase of HIV infection as suggested Bailey et al. . We hypothesize that HIV-1 would have an advantage in lymphocyte infection since HPgV may infect the same cells as HIV-1 .
The phylogenetic analysis revealed the presence of genotype 2 and the subtypes 2a and 2b in the studied population. These findings corroborate previous studies that identified these same genotypes in other regions of Brazil [18, 33, 41] and in Brazilian Amazon .
HPgV is known as a non-pathogenic virus and is not part of the routine diagnosis in the HEMOPA Foundation, but further studies are necessary to evaluate the unclear aspects related to HPgV infection especially those related to viral biology and interaction with HIV-1. This study genetically characterized and identified, by the first time, the circulating strains of HPgV among blood donors from HEMOPA Foundation and described by the first nearly complete genomes of genotype 2 in Brazilian Amazon.