Viral entry receptor

The protein on the heart muscle cell that cardiotropic viruses bind to enter.

Coxsackievirus B3 increases it.

The cause, and the door it comes through. This illness usually begins with a specific family of viruses and a specific protein on the heart cell that lets them in. 'enteroviruses and adenoviruses ARE cardiotropic and can directly infect cardiomyocytes by binding the coxsackievirus and adenovirus receptor (CAR), inducing necrosis AND/OR apoptosis through viral replication' (Front Cardiovasc Med 2026, doi 10.3389/fcvm.2026.1821475). The most frequently implicated agents are named: 'The most frequently implicated is PARVOVIRUS B19, followed by enteroviruses (e.g. coxsackieviruses and echoviruses) and adenoviruses.' and the virus does not always leave: viral genomes are reported 'in up to ~70% of patients with idiopathic dilated cardiomyopathy'. doi 10.3389/fcvm.2026.1821475

Heart muscle protein increases it.

10679478 — the virus's doorway has a second job, and it works without any virus at all. Japanese work on the autoimmune model found: '心筋ミオシン免疫のみで心筋細胞および血管内皮においてCXADR発現が誘発されその後持続する' — cardiac myosin immunization alone induces cxadr expression in cardiomyocytes and vascular endothelium, and it persists. And: 'CXADR過剰発現マウスでは、コクサッキーウイルスが感染していなくても心筋組織への炎症細胞浸潤が認められた' — in mice overexpressing it, inflammatory cells infiltrated the heart even without any coxsackievirus infection (上原記念生命科学財団研究報告集 33 (2019) — EAMにおけるCXADR発現の解析 (Uehara Memorial Foundation Research Report Vol.33, Yokohama City University)). ⇒ the mechanism is adhesion: the endothelial cxadr domain 'JAMLと異種間分子結合を形成することで、循環免疫細胞の血管内皮への遊走・接着' — it binds jaml on circulating immune cells and pulls them into the vessel wall. the same protein that lets the virus in also lets the immune system in. It is a doorway in both directions, and the source calls it '劇症型心筋炎および心筋症に対する有力な治療標的の一つ' — a promising therapeutic target for fulminant myocarditis and cardiomyopathy.

It increases Coxsackievirus B3.

The cause, and the door it comes through. This illness usually begins with a specific family of viruses and a specific protein on the heart cell that lets them in. 'enteroviruses and adenoviruses ARE cardiotropic and can directly infect cardiomyocytes by binding the coxsackievirus and adenovirus receptor (CAR), inducing necrosis AND/OR apoptosis through viral replication' (Front Cardiovasc Med 2026, doi 10.3389/fcvm.2026.1821475). The most frequently implicated agents are named: 'The most frequently implicated is PARVOVIRUS B19, followed by enteroviruses (e.g. coxsackieviruses and echoviruses) and adenoviruses.' and the virus does not always leave: viral genomes are reported 'in up to ~70% of patients with idiopathic dilated cardiomyopathy'. doi 10.3389/fcvm.2026.1821475

It increases Heart muscle inflammation.

The cause, and the door it comes through. This illness usually begins with a specific family of viruses and a specific protein on the heart cell that lets them in. 'enteroviruses and adenoviruses ARE cardiotropic and can directly infect cardiomyocytes by binding the coxsackievirus and adenovirus receptor (CAR), inducing necrosis AND/OR apoptosis through viral replication' (Front Cardiovasc Med 2026, doi 10.3389/fcvm.2026.1821475). The most frequently implicated agents are named: 'The most frequently implicated is PARVOVIRUS B19, followed by enteroviruses (e.g. coxsackieviruses and echoviruses) and adenoviruses.' and the virus does not always leave: viral genomes are reported 'in up to ~70% of patients with idiopathic dilated cardiomyopathy'. doi 10.3389/fcvm.2026.1821475

It increases The Handle on the Immune Cell.

Pmc1142417 — the virus's doorway has a second job, and it works without any virus at all. Japanese work on the autoimmune model found: '心筋ミオシン免疫のみで心筋細胞および血管内皮においてCXADR発現が誘発されその後持続する' — cardiac myosin immunization alone induces cxadr expression in cardiomyocytes and vascular endothelium, and it persists. And: 'CXADR過剰発現マウスでは、コクサッキーウイルスが感染していなくても心筋組織への炎症細胞浸潤が認められた' — in mice overexpressing it, inflammatory cells infiltrated the heart even without any coxsackievirus infection (上原記念生命科学財団研究報告集 33 (2019) — EAMにおけるCXADR発現の解析 (Uehara Memorial Foundation Research Report Vol.33, Yokohama City University)). ⇒ the mechanism is adhesion: the endothelial cxadr domain 'JAMLと異種間分子結合を形成することで、循環免疫細胞の血管内皮への遊走・接着' — it binds jaml on circulating immune cells and pulls them into the vessel wall. the same protein that lets the virus in also lets the immune system in. It is a doorway in both directions, and the source calls it '劇症型心筋炎および心筋症に対する有力な治療標的の一つ' — a promising therapeutic target for fulminant myocarditis and cardiomyopathy.

It increases Vessel wall adhesion.

PMC6881322 — The virus's doorway has a second job, and it works without any virus at all. Japanese work on the autoimmune model found: '心筋ミオシン免疫のみで心筋細胞および血管内皮においてCXADR発現が誘発されその後持続する' — cardiac myosin immunization alone induces cxadr expression in cardiomyocytes and vascular endothelium, and it persists. And: 'CXADR過剰発現マウスでは、コクサッキーウイルスが感染していなくても心筋組織への炎症細胞浸潤が認められた' — in mice overexpressing it, inflammatory cells infiltrated the heart even without any coxsackievirus infection (上原記念生命科学財団研究報告集 33 (2019) — EAMにおけるCXADR発現の解析 (Uehara Memorial Foundation Research Report Vol.33, Yokohama City University)). ⇒ the mechanism is adhesion: the endothelial cxadr domain 'JAMLと異種間分子結合を形成することで、循環免疫細胞の血管内皮への遊走・接着' — it binds jaml on circulating immune cells and pulls them into the vessel wall. the same protein that lets the virus in also lets the immune system in. It is a doorway in both directions, and the source calls it '劇症型心筋炎および心筋症に対する有力な治療標的の一つ' — a promising therapeutic target for fulminant myocarditis and cardiomyopathy. PMC6881322