Spotlight

Articles of Significant Interest in This Issue

DOI: 10.1128/JVI.00300-19

Medusavirus: a Large DNA Virus Discovered in Hot Spring Water

Yoshikawa et al. (e02130-18) discovered and isolated medusavirus, a large DNA virus with a diameter of 260 nm (T=277) and a 381-kb genome containing a full set of histone genes. The host amoeba encodes many medusavirus homologs, suggesting that lateral gene transfer occurs bidirectionally between the virus and host. The histones and other viral proteins are phylogenetically located at the root of the eukaryotic clades. Based on its morphological characteristics and phylogenomic relationships with other viruses, medusavirus appears to form a new family: Medusaviridae.

Figure1

3D reconstruction of the medusavirus particle.

JC Polyomavirus Infection Requires Endocytic Factors β-Arrestin, AP2, and Dynamin

JC polyomavirus (JCPyV) internalization requires serotonin 5-hydroxytryptamine (5-HT2) receptors and clathrin-mediated endocytosis. The endocytic machinery for JCPyV uptake is uncharacterized. Mayberry et al. (e01948-18) found that endocytic proteins β-arrestin, AP2, and GTPase dynamin 1 are required for JCPyV infection. JCPyV internalization depends on β-arrestin, a 5-HT2 receptor-binding protein, to facilitate clathrin-mediated endocytosis. These findings elucidate how JCPyV uses host cell endocytic machinery to mediate internalization and provide insight into invasion of host cells by nonenveloped viruses.

Figure2

Knockdown of β-arrestin prevents JCPyV internalization.

Herpes Simplex Virus Reactivation in the Trigeminal Ganglia and Brain Stem

Herpes simplex virus (HSV) establishes latency in neurons. Periodic reactivation events have been proposed to contribute to neurodegenerative diseases. Doll et al. (e02209-18) found infectious virus in the trigeminal ganglia (TG) and brain stem following induced reactivation in mice, but viral protein expression was detected only in TG neurons. These findings suggest that HSV reactivation primarily occurs in TG neurons and infectious virus is transported axonally from the reactivating sensory neuron to the brain stem, which offers a mechanism whereby long-term HSV infection could contribute to neurodegeneration.

Figure3

HSV reactivation in a TG neuron.

Intracellular Retinoic Acid Trafficking Pathways Regulate Hepatitis C Virus Infection

Retinoic acid (RA) inhibits viral infection by enhancing innate and adaptive immunity. However, despite enrichment of hepatocytes with RA, hepatitis C virus (HCV) can establish efficient replication. Bang et al. (e02302-18) discovered an RA-based, hepatocyte-specific, cell-intrinsic mechanism that, in association with cellular retinoic acid binding protein 1 (CRABP1), promotes HCV replication. RA-CRABP1 interaction promotes HCV replication by enhancing accumulation of lipid droplets while attenuating the antiviral action of RA. These findings reveal a new viral evasion mechanism, which exploits cellular responses to micronutrients.

Figure4

HCV replication complex on lipid droplet-associated ER membrane.

Punctuated Evolution of Myxoma Virus

The release of myxoma virus (MYXV) as a biocontrol agent against European rabbits is a canonical example of the evolution of virulence, given a constant rate of evolution in both Australia and Europe. Kerr et al. (e01994-18) found that this evolutionary constancy breaks down in recent MYXV isolates sampled from Australia. Causes of this punctuated evolution may include changes in selection pressures from prolonged drought or release of rabbit hemorrhagic disease virus as a second biocontrol approach. These findings shed light on variations in the timings of molecular clocks.

Figure5

Root-to-tip regression showing the punctuated evolution of recent MYXV.

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