Dendritic cells mediate herpes simplex virus infection and transmission through the C-type lectin DC-SIGN

Jong, Marein A. W. P. de; Witte, Lot de; Bolmstedt, Anders; Kooyk, Yvette van; Geijtenbeek, Teunis B. H.

doi:10.1099/vir.0.2008/003129-0

Cited by 72 publications

(58 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…10 Dendritic cells are known to bind to glycoproteins gB and gC present on Herpes simplex virus through DC SIGN, a C-type lectin expressed by Table 3 Table showing the severity of renal involvement and the outcome dendritic cells. 11 However, whether such an immunosuppressive effect occurs in patients with acute kidney injury is largely unknown.…”

Section: Discussionmentioning

confidence: 99%

Herpes Labialis in Patients with Russell's Viper Bite and Acute Kidney Injury: A Single Center Experience

Waikhom¹,

Sapam²,

Patil³

et al. 2011

The American Society of Tropical Medicine and Hygiene

View full text Add to dashboard Cite

Abstract. Snake bite is an important health hazard in tropical countries and is associated with significant morbidity and mortality. Herpes labialis is a common ailment caused by the Herpes simplex virus. There is no published data showing any association between the snake bite and development of Herpes labialis. Here, we present a series of patients who developed Herpes labialis after Russell's viper bite and had acute kidney injury. We attempted to find whether snake bite is an immunosuppressed state and whether it could have pre-disposed the patients to the development of these lesions.

show abstract

Section: Discussionmentioning

confidence: 99%

Herpes Labialis in Patients with Russell's Viper Bite and Acute Kidney Injury: A Single Center Experience

Waikhom¹,

Sapam²,

Patil³

et al. 2011

The American Society of Tropical Medicine and Hygiene

View full text Add to dashboard Cite

show abstract

“…Both immature and mature monocyte-derived DC express the HSV receptors nectin-1, nectin-2, and HVEM and can be infected with HSV-1 and HSV-2, but only immature monocytederived DC produce virus although at tenfold lower levels than most cell lines. Similar to HIV-1, the C-type lectin DC-SIGN functions as an attachment receptor on immature DC that enhances DC infection [58]. Mature DC are non-productively/ abortively infected [59,60].…”

Section: Subsets In Innate and Adaptive Immunity To Hsvmentioning

confidence: 99%

Langerhans cells and viral immunity

2008

Self Cite

View full text Add to dashboard Cite

Langerhans cells (LC) are a unique dendritic cell subset that are located in mucosal stratified squamous epithelium and skin epidermis. Their location is ideally suited for their function as antigen presenting cells that capture invading viruses and induce anti-viral immunity. However, it is becoming evident that the interaction between LC and viruses can result in different responses, depending on the virus and the receptors involved. Here we will discuss the recent data on the similarities and differences in roles of LC in viral immunity to and infection with HIV, herpes simplex and varicella-zoster virus. Although all three viruses interact with LC during initial infection, the effects can be quite different, reflecting differences in biology and pathogenesis. Key words: Dendritic cells Á Langerhans cells Á Infectious diseases Á HIV Á HerpesvirusesSee accompanying mini-review by Kaplan et al. Biology of LC and interactions with virusesThe resident epidermal dendritic cells (DC), Langerhans cells (LC), form a tight network with each other and with the surrounding keratinocytes via E-cadherin in the skin or mucosal stratified squamous epithelium. In the anogenital region they are distributed throughout the anogenital skin and mucosa including vagina, ectocervix as well as male foreskin. In stratified squamous epithelium, LC overlie interstitial or dermal DC [1]. LC can repopulate from local and blood-borne precursors (reviewed by Kaplan et al. in this issue [2]). Similar to other myeloid DC, LC are able to bridge innate and adaptive immunity. They are able to interact directly with microorganisms at the periphery to produce effector cytokines and initiate or restimulate activation of T and B lymphocytes through antigen presentation. LC express different pattern recognition receptors such as C-type lectin receptors (CLR) and Toll-like receptors (TLR), to bind and capture pathogens. These interactions result in activation of intracellular signalling pathways leading to LC activation and cytokine induction. The CLR expressed by skin DC differ by site: Langerin by epidermal LC and DC-SIGN and mannose receptor by dermal DC. LC like other migratory DC are in an immature, highly endocytic state while sessile in the skin/mucosa. However after pathogen binding to TLR and uptake, LC become mature and migratory, downregulating their endocytic and antigen processing capacity. Mature LC migrate to the lymph nodes where they are directly or indirectly involved in presentation of pathogenderived antigens on MHC Class I and II to T cells, resulting in activation of antigen-specific T cells [2][3][4]. Recent studies have raised the possibility that LC may have an immunosuppressive role [5][6][7]. Kaplan et al. [2] showed that contact hypersensitivity was amplified on LC ablation, while Cumberbatch et al.[5] found defective LC mobilisation in patients with psoriasis. Immunosuppression rather than stimulation could be explained, in part, by the maturational process associated with LC migration during steady-state conditions. Jian...

show abstract

“…The HSV-2 strain 333 was grown on GMK cells and harvested after 24 h of infection. Supernatant was filtrated over a 0.22-mm filter, and a plaque-titration assay was performed to determine viral titers (19). HSV-2 was inactivated by placing a Petri dish containing 3 ml viral suspension under a UV lamp for 10 min on ice.…”

Section: Cell Lines and Virusesmentioning

confidence: 99%

Herpes Simplex Virus Type 2 Enhances HIV-1 Susceptibility by Affecting Langerhans Cell Function

Jong

Witte

Taylor

et al. 2010

The Journal of Immunology

Self Cite

View full text Add to dashboard Cite

Genital herpes is the most prevalent viral sexually transmitted infection worldwide and is mainly caused by HSV type 2 (HSV-2). HSV-2 infection enhances HIV-1 susceptibility, even in the absence of clinical symptoms. In this study, we investigated the effect of HSV-2 on HIV-1 transmission by mucosal Langerhans cells (LCs). LCs are important in heterosexual transmission because they form a barrier against HIV-1 infection; LCs efficiently capture and degrade HIV-1 through the C-type lectin langerin, thereby preventing HIV-1 transmission. Notably, our data showed that HSV-2 enhanced HIV-1 infection of LCs and subsequent HIV-1 transmission to T cells. HSV-2 interfered with HIV-1 capture by langerin, which allowed efficient HIV-1 infection of LCs. HSV-2 inhibited the antiviral function of langerin at two levels; HSV-2 decreased langerin expression and competed with HIV-1 for langerin binding. HSV-2 replication was not required, because both UV-inactivated HSV-2 and TLR-3 agonist polyinosinic:polycytidylic acid similarly increased HIV-1 transmission by LCs. Therefore, we identified a mechanism by which HSV-2 enhances HIV-1 susceptibility, even in the absence of clinical symptoms. Our data demonstrated that viral coinfections, such as HSV-2, breach the protective function of LCs by abrogating langerin function, which increases HIV-1 susceptibility. These data reinforce the importance of preventing sexually transmitted infections, such as HSV-2, to reduce the transmission of HIV-1.

show abstract

Dendritic cells mediate herpes simplex virus infection and transmission through the C-type lectin DC-SIGN

Cited by 72 publications

References 44 publications

Herpes Labialis in Patients with Russell's Viper Bite and Acute Kidney Injury: A Single Center Experience

Herpes Labialis in Patients with Russell's Viper Bite and Acute Kidney Injury: A Single Center Experience

Langerhans cells and viral immunity

Herpes Simplex Virus Type 2 Enhances HIV-1 Susceptibility by Affecting Langerhans Cell Function

Contact Info

Product

Resources

About