Herpesviruses

Nuclear Egress and Envelopment of HSV

from Joel D. Baines writing in Alphaherpesviruses: Molecular Virology:

In a process unique in biology, all herpesviruses obtain their initial virion envelope by budding through the inner nuclear membrane. In the most prominent model of virion egress, the envelope of the perinuclear virion then fuses with the luminal surface of the outer nuclear membrane, releasing the de-enveloped capsid into the cytosol for subsequent budding events. The pUL31/pUL34 protein complex is a major player in the initial budding event, and mediates several relevant functions including disruption of the nuclear lamina, recruitment of other viral proteins to the inner nuclear membrane and perinuclear virion, and budding of the nucleocapsid through the inner nuclear membrane.

Further reading: Alphaherpesviruses: Molecular Virology

Autophagy

Autophagy is a rapidly growing area of biomedical research with broad relevance to fields including microbiology, cell biology, immunology, cancer biology, and neurodegeneration. In infection and immunity, it is emerging as a pivotal pathway mediating direct pathogen degradation as well as for the development of robust innate and adaptive immune responses. Successful pathogens have evolved to either evade or harness the autophagy pathway to further their replication and pathogenesis. In a recent review the basic aspects of autophagy will be described, along with its role in cellular homeostasis, and the development of immunity. The primary focus is a survey of past and recent research defining the interplay of autophagy and the herpesviruses, with particular reference to immune evasion and pathogenesis.

Further reading: Alphaherpesviruses: Molecular Virology

Human Alpha-herpesvirus MicroRNAs

MicroRNAs (miRNAs) are an extensive class of approx 22 nucleotide long regulatory RNAs expressed by all mammalian cells and also by several DNA viruses, including many members of the herpesvirus family. Using deep sequencing technology, it has now been demonstrated that Herpes Simplex Virus 1 (HSV-1) encodes at least eight viral miRNAs, seven of which are expressed in latently infected human neurons. Similarly, HSV-2 has also been shown to encode at least six miRNAs, four of which are evolutionarily conserved between HSV-2 and HSV-1. Perhaps surprisingly, varicella zoster virus does not appear to express any viral miRNAs in latently infected cells. A recent review discusses the potential functions of the currently known HSV-1 and HSV-2 miRNAs, focusing on a possible role in stabilizing viral latency in infected neurons.

Further reading: Alphaherpesviruses: Molecular Virology