A global perspective on hantavirus ecology, epidemiology, and disease

Abstract

Hantaviruses are enzootic viruses that maintain persistent infections in their rodent hosts without apparent disease symptoms. The spillover of these viruses to humans can lead to one of two serious illnesses, hantavirus pulmonary syndrome and hemorrhagic fever with renal syndrome. In recent years, there has been an improved understanding of the epidemiology, pathogenesis, and natural history of these viruses following an increase in the number of outbreaks in the Americas. In this review, current concepts regarding the ecology of and disease associated with these serious human pathogens are presented. Priorities for future research suggest an integration of the ecology and evolution of these and other host-virus ecosystems through modeling and hypothesis-driven research with the risk of emergence, host switching/spillover, and disease transmission to humans.

FIG. 1.

Tomography of an HTNV virion particle. Shown is a near-tangential section through a tomographic reconstruction of a virion. A set of parallel rod-like densities (indicated by green arrows) can be seen beneath the membrane. Anisotropy is in the direction perpendicular to the page. The section is 5.1 nm thick, and the scale bar represents 25 nm. The tomogram was denoised by using nonlinear anisotropic diffusion as implemented in BSOFT (142a). (Photograph courtesy of Anthony J. Battisti and Paul R. Chipman, Purdue University; reproduced with permission.)

FIG. 2.

The hantavirus life cycle. The basic steps include the attachment of the virion particle to the cell's surface through interactions between the host's cell surface receptors and the viral glycoprotein (1); entry through the use of receptor-mediated endocytosis and the uncoating and release of the viral genomes immediately thereafter (2); transcription of complementary RNA (cRNA) from the viral RNA (vRNA) genome using host-derived primers (3); translation of L, M, and S mRNAs into viral proteins using host machinery (4); replication and amplification of vRNA, assembly with the N protein, and transport to the Golgi apparatus (5); assembly of all components at the Golgi apparatus or, possibly for New World viruses, at the plasma membrane (alternative assembly) (6); and viral egress via the fusion of the Golgi vesicle harboring the mature virion particles with the plasma membrane (7).

FIG. 3.

Geographical representation of approximate hantaviral disease incidence by country per year. (Courtesy of Douglas Goodin, Kansas State University; reproduced with permission.)

FIG. 4.

Phylogenetic tree of representative hantaviruses from the Old and New Worlds. (Courtesy of Yong-kyu Chu, University of Louisville; reproduced with permission.)