Herpesvirus Infections and Treatments

This study shows that both neutralization and effector functions of antibodies are needed for effective protection against neonatal HSV-1, while effector functions alone suffice for HSV-2.

This study compares a novel VZV mRNA vaccine (ZOSAL) with Shingrix in mice and rhesus macaques, showing ZOSAL induces stronger T cell immunity and safety.

The study identifies a suppressor mutation in HSV-1 NEC that stabilizes the hexagonal lattice, restoring membrane budding in various mutants.

This study shows c-Jun signaling during HSV-1 initial infection promotes latency and enhances later reactivation by facilitating the transition from Phase I to Phase II reactivation.

This study shows HSV pUL16 and pUL21 proteins block nucleocapsid docking at nuclear pore complexes, preventing genome re-entry into the nucleus.

This study reconstitutes HSV-1 membrane fusion in vitro and identifies low pH as a co-trigger, along with a host receptor, for efficient fusion.

This paper identifies a non-enzymatic role for murine gammaherpesvirus 68 vUNG in forming a complex with viral DNA replication factors, independent of its catalytic activity.

The paper presents ancient HSV-1 genomes from Europe, estimates mutation rates, and suggests lineage replacement during the Bronze Age.

This study identifies US3 kinase's role in promoting retrograde transport of nucleocapsids in axons via Akt/mToRC1 signaling during alpha herpesvirus infection.

This study identifies ICP22 as a viral repressor of cellular RNA polymerase II transcription elongation by interacting with elongation factors, and suggests VP16 may compete with ICP22 for these factors.

This study shows that HSV-1 protein ICP4 both activates and represses host gene transcription by modulating RNA polymerase II occupancy and promoter pausing.

This study shows that the Us9 protein of pseudorabies virus regulates axonal sorting differently in immature versus mature neurons, with immature neurons showing reduced Us9-dependent sorting and increased Us9-independent transport.

The paper reports a case of HSV mistyping caused by HSV-1 x HSV-2 recombination in the UL27 gene, which is important for diagnostics and therapeutics.

This study investigates how HSV-1 latency affects VGSC activity in DRG neurons, finding reduced activity during acute infection and increased activity during latency.

The paper uses single-cell RNA-sequencing to study HSV-1 infection in human fibroblasts, identifying NRF2 activation as an antiviral response that reduces virus production.

This study identifies HSV-1 ICP4 as a key factor in recruiting host transcription machinery to the viral genome, leading to host transcriptional shut off.

This study uses consensus clustering of HSV1 protein interaction networks to uncover evolutionary links between herpesviruses and bacteriophages, identifying pUS10 as a potential evolutionary vestige.

The paper shows that Topoisomerase 2-dependent DNA damage and AKT phosphorylation dynamics regulate HSV-1 latency by integrating extracellular signals and nuclear DNA damage.

The paper develops tools to directly sequence HSV genomes from clinical samples with high sensitivity and low viral load, revealing limited evolution during cell culture.

The paper uses dynamic proteomics to study HSV1 infection in individual cells, finding preexisting cell-state differences influence infection outcomes.