The herpes simplex virus 1 U(S)3 regulates phospholipid synthesis

Area of Science:

• Virology
• Cell Biology
• Molecular Biology

Background:

• Herpes simplex virus type 1 (HSV-1) requires host cell membranes for envelopment.
• The viral protein U(S)3 is implicated in modulating host cell processes during infection.

Purpose of the Study:

• To investigate the role of U(S)3 in phospholipid metabolism and membrane dynamics during HSV-1 infection.
• To quantify membrane changes associated with viral envelopment in the absence of U(S)3.

Main Methods:

• Cell cultures infected with wild-type HSV-1 and a U(S)3 deletion mutant (R7041ΔU(S)3).
• Quantification of [(3)H]-choline incorporation into cellular membranes.
• Measurement of nuclear membrane surface area and viral envelope formation.
• Assessment of Golgi complex morphology.

Main Results:

• [(3)H]-choline incorporation into nuclear and cytoplasmic membranes was enhanced in R7041ΔU(S)3 infected cells.
• Nuclear membranes formed extensive folds (~45% of nuclear surface) in R7041ΔU(S)3 infected cells.
• Significant viral envelope formation (~2400 virions/cell) and dramatic Golgi expansion were observed during R7041ΔU(S)3 infection.

Conclusions:

• The viral protein U(S)3 plays a critical role in regulating host cell membrane biosynthesis during HSV-1 infection.
• Absence of U(S)3 disrupts normal membrane turnover, leading to aberrant membrane structures and Golgi alterations.
• These findings highlight U(S)3's importance in coordinating viral replication with host cell membrane dynamics.