Langerhans Cells and Recurrent Infection with Herpes Simplex Virus

1991 ◽  
pp. 185-201 ◽  
Author(s):  
N. A. Williams ◽  
W. A. Blyth ◽  
T. J. Hill
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Langerhans Cells ◽  
Recurrent Infection ◽  
Simplex Virus

Perinatal Herpes Simplex Virus Infections

PEDIATRICS ◽  
1980 ◽  
Vol 66 (1) ◽  
pp. 147-149
Author(s):  
Alfred W. Brann ◽  
Robert T. Hall ◽  
Rita G. Harper ◽  
George A. Little ◽  
M. Jeffrey Maisels ◽  
...  
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Recurrent Infection ◽  
Case Fatality ◽  
Virus Infections ◽  
Mortality And Morbidity ◽  
Relative Paucity ◽  
Source Of Infection ◽  
Simplex Virus ◽  
Hsv Infections

Because of the relative paucity of data on the epidemiology and management of perinatal herpes simplex virus (HSV) infections, the following recommendations represent the best current judgments of the Committees on Fetus and Newborn and Infectious Diseases of the American Academy of Pediatrics. HSV infection of the newborn is associated with a case fatality rate of 60% and at least half of the survivors have significant neurologic or ocular sequelae, or both. Approximately 75% of isolates from affected neonates are HSV-2 and 25% are HSV-1. Although preliminary data suggest that antiviral chemotherapy is effective in reducing mortality and morbidity resulting from neonatal HSV infections, measures designed to prevent infection of newborns are currently the most important means of controlling neonatal infections. A maternal source of infection can be found in about 90% of neonatal cases. Maternal HSV infection is usually caused by type 2 strains and involves the labia, cervix, and/or vagina. The majority of genital infections are asymptomatic and difficult to recognize on clinical examination, making identification of women whose infants are in jeopardy very difficult. EPIDEMIOLOGY Maternal Infection Primary HSV infection during pregnancy may be associated with spontaneous abortion, prematurity, and rarely with congenital anomalies. The risk of infection to the newborn appears to be the highest in primary genital infection of the pregnant woman, but is also high in recurrent infection. Women with a history of recurrent genital HSV infection, those with active disease during the current pregnancy, and those whose sexual partners have proven genital HSV infection should be monitored with virologic or cytologic studies, or both, at least twice during the last six weeks of pregnancy.

Quantitative studies on langerhans cells in mouse corneal epithelium following infection with herpes simplex virus

1987 ◽  
Vol 45 (1) ◽  
pp. 127-140 ◽  
Author(s):  
S.J. Lewkowicz-Moss ◽  
C. Shimeld ◽  
K. Lipworth ◽  
T.J. Hill ◽  
W.A. Blyth ◽  
...  
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Corneal Epithelium ◽  
Langerhans Cells ◽  
Quantitative Studies ◽  
Simplex Virus

scholarly journals Herpes Simplex Virus type 1 infects Langerhans cells and the novel epidermal dendritic cell, Epi-cDC2s, via different entry pathways

2021 ◽  
Vol 17 (4) ◽  
pp. e1009536
Author(s):  
Kirstie M. Bertram ◽  
Naomi R. Truong ◽  
Jacinta B. Smith ◽  
Min Kim ◽  
Kerrie J. Sandgren ◽  
...  
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Langerhans Cells ◽  
Vaccine Development ◽  
Mononuclear Phagocytes ◽  
The Novel ◽  
Endosomal Acidification ◽  
Simplex Virus ◽  
Hsv 1

Skin mononuclear phagocytes (MNPs) provide the first interactions of invading viruses with the immune system. In addition to Langerhans cells (LCs), we recently described a second epidermal MNP population, Epi-cDC2s, in human anogenital epidermis that is closely related to dermal conventional dendritic cells type 2 (cDC2) and can be preferentially infected by HIV. Here we show that in epidermal explants topically infected with herpes simplex virus (HSV-1), both LCs and Epi-cDC2s interact with HSV-1 particles and infected keratinocytes. Isolated Epi-cDC2s support higher levels of infection than LCs in vitro, inhibited by acyclovir, but both MNP subtypes express similar levels of the HSV entry receptors nectin-1 and HVEM, and show similar levels of initial uptake. Using inhibitors of endosomal acidification, actin and cholesterol, we found that HSV-1 utilises different entry pathways in each cell type. HSV-1 predominantly infects LCs, and monocyte-derived DCs, via a pH-dependent pathway. In contrast, Epi-cDC2s are mainly infected via a pH-independent pathway which may contribute to the enhanced infection of Epi-cDC2s. Both cells underwent apoptosis suggesting that Epi-cDC2s may follow the same dermal migration and uptake by dermal DCs that we have previously shown for LCs. Thus, we hypothesize that the uptake of HSV and infection of Epi-cDC2s will stimulate immune responses via a different pathway to LCs, which in future may help guide HSV vaccine development and adjuvant targeting.

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