Research Article: PARV4: An Emerging Tetraparvovirus

Date Published: May 1, 2014

Publisher: Public Library of Science

Author(s): Philippa C. Matthews, Amna Malik, Ruth Simmons, Colin Sharp, Peter Simmonds, Paul Klenerman, Richard C. Condit.

http://doi.org/10.1371/journal.ppat.1004036

Abstract

Partial Text

PARV4 was first reported in 2005 in a hepatitis B virus–infected injecting drug user (IDU) [1]. It was detected by a screening process that aimed to identify new DNA viruses in subjects reporting risk factors for HIV combined with nonspecific symptoms of “viral infection syndrome”, including fatigue, malaise, and headache [1].

PARV4 isolates have been subclassified into three genotypes (Figure 1B). Genotypes 1 and 2 (the latter originally termed PARV5) are predominant in Europe, North America, and Asia [3], [4]; genotype 3 is most widespread in Africa [5], [6]. Genetic diversity within each genotype is minimal, leading to one possible inference that the spread of each has been a relatively recent phenomenon, likely originating within the past 20–30 years [4]. It is possible that the three genotypes represent separate zoonotic transmissions of PARV4 into human populations, perhaps from chimpanzees and monkey species that harbour the most closely related parvoviruses to PARV4 [4], [7]. However, in a recent study [8], the nonhuman PARV4-like variants were species-specific, despite frequent opportunities for transmission, including blood contact, between nonhuman primates and human hunters. Despite its scarcity in Western countries, PARV4 may, alternatively, represent the human lineage of a parvovirus that has remained species-specific throughout the evolution of the Partetravirus genus.

There is currently no definitive clinical syndrome associated with PARV4 infection, and the potential pathogenicity of related hokoviruses in animals is also unknown [17]. In the majority of instances, PARV4 viraemia appears to be self-limiting and asymptomatic [6], and there is no consistent association with increased severity of co-existing blood-borne viruses [3].

Evidence of PARV4 infection is most frequently detected by an ELISA for specific IgG antibody to VP-2 [11]. This response appears to be sustained over time, as with other parvovirus infections; weak or transient VP-2 IgM positivity has also been reported in acute infection [11].

Like other human parvoviruses, PARV4 has the potential for persistence: DNA can be extracted from tissue long (indeed, possibly life-long) after primary infection [4], [19]. This is also supported by a high frequency and magnitude of T-cell responses to PARV4 (detected in vitro by Interferon-gamma ELISpot assays) [20], similar to that which is seen in response to other chronic or latent viral infections—the best characterised examples being the herpesviruses CMV and EBV.

Despite the lack of consistent evidence for PARV4-mediated disease, there are several concerns about the implications of this virus.

 

Source:

http://doi.org/10.1371/journal.ppat.1004036

 

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