Herpesvirus entry mediator: Difference between revisions

Latest revision as of 04:37, 29 December 2024

Herpesvirus entry mediator (HVEM) is a protein that in humans is encoded by the TNFRSF14 gene. HVEM is a member of the tumor necrosis factor receptor superfamily and plays a crucial role in the immune system by mediating the entry of herpesvirus into cells.

Function[edit]

HVEM is a cell surface receptor that interacts with several ligands, including herpes simplex virus glycoprotein D (gD), lymphotoxin-alpha, and LIGHT. These interactions are important for the regulation of immune responses, inflammation, and cell death. HVEM is involved in the activation of NF-kB and JNK pathways, which are critical for cell survival and proliferation.

Clinical significance[edit]

The interaction between HVEM and herpes simplex virus gD is essential for the virus to enter host cells, making HVEM a potential target for therapeutic intervention in herpesvirus infections. Additionally, HVEM has been implicated in various autoimmune diseases and cancers, where its expression and signaling pathways may contribute to disease progression.

Interactions[edit]

HVEM interacts with several proteins, including:

BTLA (B and T lymphocyte attenuator)
CD160
LIGHT (TNFSF14)
Lymphotoxin-alpha

These interactions modulate immune responses and can either stimulate or inhibit immune cell activity, depending on the context.

References[edit]

External links[edit]

@@ Line 1: / Line 1: @@
-'''Herpesvirus entry mediator''' ('''HVEM'''), also known as '''TNFRSF14''' (tumor necrosis factor receptor superfamily member 14), is a protein that in humans is encoded by the TNFRSF14 gene. It is a member of the [[tumor necrosis factor receptor]] superfamily and plays a key role in the entry of [[herpesvirus]] into cells.
-== Structure ==
+{{Infobox protein
-The HVEM protein is a type I membrane protein that is expressed in many [[immune cells]], including [[T cells]], [[B cells]], and [[monocytes]]. It consists of an extracellular domain containing four cysteine-rich repeats, a transmembrane domain, and a cytoplasmic domain that contains a death domain motif.
+| name = Herpesvirus entry mediator
+| image = <!-- Image removed -->
+| caption = <!-- Caption removed -->
+| symbol = HVEM
+| HGNCid = 11939
+| OMIM = 602870
+| PDB = 1JMA
+| RefSeq = NM_003820
+| UniProt = Q92956
+}}
+'''Herpesvirus entry mediator''' ('''HVEM''') is a [[protein]] that in humans is encoded by the '''TNFRSF14''' gene. HVEM is a member of the [[tumor necrosis factor receptor superfamily]] and plays a crucial role in the [[immune system]] by mediating the entry of [[herpesvirus]] into cells.
 == Function ==
-HVEM acts as a receptor for [[herpes simplex virus]] (HSV) and [[pseudorabies virus]] (PRV), facilitating their entry into cells. It interacts with the viral glycoprotein D (gD), which is present on the surface of the virus. This interaction triggers a series of events that lead to the fusion of the viral envelope with the cell membrane, allowing the virus to enter the cell.
+HVEM is a cell surface receptor that interacts with several ligands, including [[herpes simplex virus]] glycoprotein D (gD), [[lymphotoxin-alpha]], and [[LIGHT]]. These interactions are important for the regulation of [[immune responses]], [[inflammation]], and [[cell death]]. HVEM is involved in the activation of [[NF-kB]] and [[JNK]] pathways, which are critical for [[cell survival]] and [[proliferation]].
-In addition to its role in viral entry, HVEM also plays a role in immune regulation. It can interact with several ligands, including LIGHT and BTLA, to modulate immune responses. For example, the interaction between HVEM and BTLA can inhibit T cell activation, providing a mechanism for immune tolerance.
 == Clinical significance ==
-Mutations in the TNFRSF14 gene can lead to a variety of immune disorders. For example, loss-of-function mutations have been associated with an increased risk of [[autoimmune diseases]], such as [[rheumatoid arthritis]] and [[lupus]]. On the other hand, gain-of-function mutations can lead to the development of certain types of [[cancer]], including [[non-Hodgkin lymphoma]] and [[cutaneous T cell lymphoma]].
+The interaction between HVEM and herpes simplex virus gD is essential for the virus to enter host cells, making HVEM a potential target for therapeutic intervention in [[herpesvirus infections]]. Additionally, HVEM has been implicated in various [[autoimmune diseases]] and [[cancers]], where its expression and signaling pathways may contribute to disease progression.
-== Research ==
+== Interactions ==
-Research is ongoing to develop drugs that can block the interaction between HVEM and its ligands, with the aim of preventing herpesvirus infection or modulating immune responses. Several small molecule inhibitors and monoclonal antibodies are currently in preclinical or early clinical development.
+HVEM interacts with several proteins, including:
+* [[BTLA]] (B and T lymphocyte attenuator)
+* [[CD160]]
+* [[LIGHT]] (TNFSF14)
+* [[Lymphotoxin-alpha]]
-[[File:Herpesvirus_entry_mediator.png|thumb|right|Structure of the herpesvirus entry mediator protein.]]
+These interactions modulate immune responses and can either stimulate or inhibit immune cell activity, depending on the context.
 == See also ==
-* [[Herpesvirus]]
-* [[Tumor necrosis factor receptor]]
 * [[Herpes simplex virus]]
-* [[Pseudorabies virus]]
+* [[Tumor necrosis factor receptor superfamily]]
+* [[Immune system]]
 == References ==
-<references />
+{{Reflist}}
-[[Category:Proteins]]
+== External links ==
-[[Category:Virology]]
+* [https://www.ncbi.nlm.nih.gov/gene/8764 TNFRSF14 gene - NCBI]
-[[Category:Immunology]]
+* [https://www.uniprot.org/uniprot/Q92956 UniProt entry for HVEM]
-[[Category:Medicine]]
-{{medicine-stub}}
+[[Category:Human proteins]]
+[[Category:Immune system]]
+[[Category:Herpesviridae]]
+[[Category:Tumor necrosis factor receptor superfamily]]