A herpes simplex virus 1 recombinant lacking the glycoprotein G coding sequences is defective in entry through apical surfaces of polarized epithelial cells in culture and in vivo.
A herpes simplex virus 1 recombinant lacking the glycoprotein G coding sequences is defective in entry through apical surfaces of polarized epithelial cells in culture and in vivo.
复制标题
缺乏糖蛋白G编码序列的单纯疱疹病毒1重组体在通过培养物和体内极化上皮细胞的顶面进入时存在缺陷。
DOI:
10.1073/pnas.020510297
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发表时间:
2000
影响因子:
11.1
通讯作者:
Sears,AE
中科院分区:
文献类型:
--
作者:
Tran,LC;Kissner,JM;Westerman,LE;Sears,AE
During infection of a new host, the first surfaces encountered by herpes simplex viruses are the apical membranes of epithelial cells of mucosal surfaces. These cells are highly polarized, and the protein composition of their apical and basolateral membranes are very different, so that different viral entry pathways have evolved for each surface. To determine whether the viral glycoprotein G (gG) is specifically required for efficient infection of a particular surface of polarized cells, apical and basal surfaces were infected with wild-type virus or a gG deletion mutant. After infection of polarized cells in culture, the gG−virus was deficient in infection of apical surfaces but was able to infect cells through basal membranes, replicate, and spread into surrounding cells. The gG-dependent step in apical infection was a stage beyond attachment. Afterin vivoinfection of apical surfaces of epithelial cells of nonscarified mouse corneas, infection by glycoprotein C−or gG−virus was considerably reduced as compared with that observed after infection with wild-type virus. In contrast, when corneas were scarified, allowing virus access to other cell surfaces, the gG and glycoprotein C deletion mutants infected eyes as efficiently as wild-type viruses. A secondary mutation allowing infection of apical surfaces by gG−virus arose readily during passage of the virus in nonpolarized cells, indicating that either the gG-dependent step of apical infection can be bypassed or that another viral protein can acquire the same function.
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影响因子:
3.8
作者:
HEROLD, BC;VISALLI, RJ;SPEAR, PG
通讯作者:
SPEAR, PG
影响因子:
5.4
作者:
JOHNSON, DC;LIGAS, MW
通讯作者:
LIGAS, MW
DOI:
10.1126/science.3033824
发表时间:
1987
期刊:
Science (New York, N.Y.)
影响因子:
--
作者:
Weber,PC;Levine,M;Glorioso,JC
通讯作者:
Glorioso,JC
影响因子:
3.7
作者:
Kousoulas,KG;Pellett,PE;Pereira,L;Roizman,B
通讯作者:
Roizman,B