Human Gyrovirus DNA in Human Blood, Italy - Vol. 18 No. 6 - June 2012 - Emerging Infectious Disease journal - CDC
Volume 18, Number 6–June 2012
Volume 18, Number 6—June 2012
Human Gyrovirus DNA in Human Blood, Italy
In 2011, Sauvage et al. reported the discovery of a novel virus in human skin specimens and named it human gyrovirus (HGyV) (1). The characteristics of its genome—a single, closed molecule of circular, negative-sense DNA ≈2,300 nt long—and sequence homology with the chicken anemia virus (CAV) have suggested that HGyV might be the first human-infecting member of the genus Gyrovirus, which is part of the family Circoviridae and encompasses only 1 previously known species, CAV (2).
Human gyrovirus (HGyV) is a recent addition to the list of agents found in humans. Prevalence, biologic properties, and clinical associations of this novel virus are still incompletely understood. We used qualitative PCRs to detect HGyV in blood samples of 301 persons from Italy. HGyV genome was detected in 3 of 100 solid organ transplant recipients and in 1 HIV-infected person. The virus was not detected in plasma samples from healthy persons. Furthermore, during observation, persons for whom longitudinal plasma samples were obtained had transient and scattered presence of circulating HGyV. Sequencing of a 138-bp fragment showed nucleotide identity among all the HGyV isolates. These results show that HGyV can be present in the blood of infected persons. Additional studies are needed to investigate possible clinical implications.
The genome of HGyV, which resembles CAV more closely than other members of the family (1,3), contains an untranslated region of ≈380 nt and 3 major partially overlapping open reading frames (named viral protein [VP] 1, VP2, and VP3) that encode proteins of 465, 231, and 31 aa, respectively. Whether HGyV and equivalent CAV proteins have similar functions is unknown. VP3 products of HGyV and CAV (for which the coded protein has been named apoptin) share short, functionally pivotal amino acid motifs, suggesting that HGyV also encodes an apoptin-like protein. The CAV apoptin induces tumor-specific apoptosis in a p53-independent fashion and has been shown to be a potential anticancer therapeutic agent in various animal models (4–8).
The epidemiology, biologic properties, and pathogenic potential of HGyV remain poorly understood. Sauvage et al. (1) detected the HGyV genome in nonlesional skin specimens of healthy persons and 1 HIV-positive patient but not in respiratory and fecal samples. This observation suggests that HGyV is most likely part of the normal skin microflora of humans, similarly to other recently discovered viruses (9,10). However, like related animal viruses, CAV infects a large range of cell types and causes a variety of pathologies (including bone marrow aplasia leading to aplastic anemia, hemorrhage, and lymphoid depletion) and increased death in young chicken (11). Also, CAV infection has been associated with the worsening of pathologies caused by other viral and bacterial agents (11–13).
Thus, because HGyV might cause clinically relevant disorders, guidance in choosing the directions for clinical investigation is crucial and needs to come from studies aimed at defining the prevalence of HGyV infection in different human populations, portal of entry, type of cells targeted during primary amplification, and site of latency/persistence. We investigated the presence of HGyV DNA in blood samples of 301 persons in Italy using specific PCRs. The results indicated overall HGyV positivity of 1.3%.