Conformational Changes in the Nuclear Lamina Induced by Herpes Simplex Virus Type 1 Require Genes UL31 and UL34

摘要: The herpes simplex virus type 1 (HSV-1) U L 31 and 34 proteins are dependent on each other for proper targeting to the nuclear membrane required efficient envelopment of nucleocapsids at inner membrane. In this work, we show that whereas solubility lamins A C (lamin A/C) was not markedly increased, HSV induced conformational changes in lamina infected cells, as viewed after staining with three different lamin A/C-specific antibodies. one case, reactivity a monoclonal antibody recognizes an epitope tail domain greatly reduced HSV-infected cells. This apparent HSV-induced masking both 34, but these were sufficient mask uninfected indicating also required. second rabbit polyclonal primarily epitopes A/C rod revealed is decreased availability reaction antibody, protein dispensable effect. Still another indicated virtually no difference versus more than result depletion rim. Further evidence supporting interaction between 31/U complex includes observations (i) overexpression cells relocalize from rim into nucleoplasmic aggregates, (ii) some cytoplasm, (iii) could directly bind vitro. These studies suggest modify conformation possibly by direct A/C, likely involved. Given potentially excludes sites membrane, alteration may reflect role perturbing promote nucleocapsid egress nucleus. Alternatively, data compatible