It remains unclear how far HBoV contributes to respiratory and/or gastrointestinal disease. More and more evidence supports the assumption that HBoV is indeed an infectious and contagious agent, but a chance remains that it solely synergistically increases the clinical severity of other infections. Consequently, well planned and designed clinical studies with sophisticated case controls need to be performed in order to finally rule out the role of bocavirus, unless animal or at least in vitro models demonstrate its pathogenicity.  Plasmacytoid Dendritic Cells and the Control of Herpesvirus Infections Type-I interferons (IFN-I) are cytokines essential for vertebrate antiviral defense, including against herpesviruses. IFN-I have potent direct antiviral activities and also mediate a multiplicity of immunoregulatory functions, which can either promote or dampen antiviral adaptive immune responses. Plasmacytoid dendritic cells (pDCs) are the professional producers of IFN-I in response to many viruses, including all of the herpesviruses tested. There is strong evidence that pDCs could play a major role in the initial orchestration of both innate and adaptive antiviral immune responses. Depending on their activation pattern, pDC responses may be either protective or detrimental to the host. Here, we summarize and discuss current knowledge regarding pDC implication in the physiopathology of mouse and human herpesvirus infections, and we discuss how pDC functions could be manipulated in immunotherapeutic settings to promote health over disease. Herpesviruses are enveloped viruses, with genomes consisting in double-stranded linear DNA. Nine herpesviruses have currently been associated with diseases in humans (Table 1 ). Three herpesviruses have been identified in mice. Herpesviruses establish life-long persistent infections in their natural hosts, with a very high seroprevalence ranging from 30% to 90% depending on the country and on the virus. The infection is usually asymptomatic in immunocompetent individuals. Upon resolution of the acute phase of the primary infection, herpesviruses establish latent infection in specific cell types. A variety of stress conditions, including immunosuppression or inflammation, promote herpesvirus reactivation which can eventually lead to severe pathology (for review see [1] ). Indeed, herpesviruses are some of the most common opportunistic agents encountered in AIDS patients and in recipients of bone marrow or solid organ transplantation. Herpesviruses harbor a very selective tropism for their host species, attesting to a very long history of co-evolution spanning several millions of years. The mouse cytomegalovirus (MCMV) cannot infect rats or humans, and reciprocally for the human or rat CMVs. The genome of herpesviruses is of considerable size and complexity as compared to that of many other viruses. Herpesviruses harbor a high number of genes that are not essential for their replicative cycle but that appear to have been selected for escape from, or hijacking of, the host immune system. However, reciprocally, the immune systems of the hosts have evolved counterstrategies to control the viruses. One of the earliest and most potent responses of the hosts to infections with herpesviruses is the production of type-I interferons (IFN-I).