Future Virology最新文献

Rocahepevirus ratti (rat HEV) has become a zoonotic pathogen of growing public health concern. First identified in 2010 in wild rats in Germany, Rocahepevirus ratti-C1 (HEV-C1) was genetically distinct from Paslahepevirus genotypes that cause hepatitis E in humans. Although early research indicated that HEV-C1 could not infect non-human primates, reports of human infections in Hong Kong circa 2018 raised the possibility of a new zoonoses. Currently, 23 known human instances of rat HEV infection have been reported, affecting both immunocompetent and immunocompromised individuals. A critical review of the current knowledge regarding rat HEV, including its epidemiology, zoonotic spillover, health implications, and knowledge gaps with future research directions is presented in this paper. Here we describe possible modes of transmission, human pathophysiology, and clinical signs and symptoms in infected people. The need for diagnostic tools specific for rat HEV, current detection limitations, and diagnostic challenges are also discussed. We explore potential implications for public health, stressing the value of rodent control, surveillance, and preventive measures. Knowledge gaps in the field of rat HEV research are highlighted and future lines of inquiry to reduce the potential risks to public health posed by this emerging zoonotic virus are discussed.

Polyomaviruses (PyVs) are widespread commensals among vertebrates, including humans, where they silently persist lifelong in healthy hosts. Polyomavirus infection in immunocompromised individuals can cause life-threatening diseases. Of the 14 human polyomaviruses discovered to date, resurgent infections by the JC and BK PyVs are responsible for high morbidity and mortality in individuals with certain inherited or acquired immune perturbations. JCPyV causes several brain disorders, the most fully characterized and of highest (albeit rare) incidence being Progressive Multifocal Leukoencephalopathy (PML). BKPyV infection elicits a diffuse interstitial nephritis in up to 10% of allograft kidneys, and approximately 10% of allogeneic hematopoietic stem cell transplant recipients develop BKPyV-associated hemorrhagic cystitis. No clinically efficacious anti-PyV agents are available. Because PyVs are species-specific, determinants of pathogenesis by human PyVs are inferred from infection of cells in tissue culture. Insights into viral and immunological factors that enable PyVs to persist and cause central nervous system (CNS) and kidney disease in vivo have emerged from recent studies using mouse PyV (MuPyV), a natural murine pathogen. In this perspective, we discuss recent findings using the MuPyV-mouse model to understand early immunovirologic events of CNS and kidney infection, the development of PyV antiviral agents, and promising research directions for polyomavirology.

The cells infected by a virus in vivo are critical determinants of infection and disease. These same susceptible cells can also provide a wide range of options for viral propagation. The type of cell used to produce a virus, i.e. the producer cell type, can change the macromolecular composition of viruses and other factors associated with viral inoculum independent of genetic selection. Changes in the post-translational modifications of viral proteins, virion protein and lipid composition, and the types of viral structures released from different producer cells have been observed for several virus families. These producer cell-dependent changes can have wide ranging consequences on subsequent infection by altering viral tropism, antigenicity, and overall infectious capacity. The changes imparted by the producer cell impact experimental outcomes and influence viral spread and disease in vivo. In this review, we discuss the literature documenting the effects that producer cell type has on the macromolecular composition and infectious properties of virions and viral inoculum. We discuss the evidence of producer cell-dependent changes on the outcome of infection and antigenicity from diverse viral families. These observations highlight the need to better understand the impact producer cell type has on viral infections and disease.