Host Calcium Channels and Pumps in Viral Infections, 2020, Chen et al

[Hutan]

Host Calcium Channels and Pumps in Viral Infections
Xingjuan Chen,1,2 Ruiyuan Cao,2,* and Wu Zhong2,*

Ca2+ is essential for virus entry, viral gene replication, virion maturation, and release. The alteration of host cells Ca2+ homeostasis is one of the strategies that viruses use to modulate host cells signal transduction mechanisms in their favor.

Host calcium-permeable channels and pumps (including voltage-gated calcium channels, store-operated channels, receptor-operated channels, transient receptor potential ion channels, and Ca2+-ATPase) mediate Ca2+ across the plasma membrane or subcellular organelles, modulating intracellular free Ca2+. Therefore, these Ca2+ channels or pumps present important aspects of viral pathogenesis and virus–host interaction. It has been reported that viruses hijack host calcium channels or pumps, disturbing the cellular homeostatic balance of Ca2+. Such a disturbance benefits virus lifecycles while inducing host cells’ morbidity.

Evidence has emerged that pharmacologically targeting the calcium channel or calcium release from the endoplasmic reticulum (ER) can obstruct virus lifecycles. Impeding virus-induced abnormal intracellular Ca2+ homeostasis is becoming a useful strategy in the development of potent antiviral drugs. In this present review, the recent identified cellular calcium channels and pumps as targets for virus attack are emphasized.

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[Hutan]

It seems that this disruption of cell's calcium processes is common in viruses.

It has been demonstrated that the host cell dysfunction following infection with a virus is accompanied by abnormal intracellular Ca2+concentration [3]. A virus can hijack the host intracellular Ca2+ system to achieve successful replication via multiple routes; for instance, viral proteins directly bind to Ca2+ or disturb the membrane permeability for Ca2+ by manipulating Ca2+ apparatus.

A recent SARS-CoV-2 study noted that the virus affects calcium signalling in endothelial cells. Endothelial cells, especially in the muscles and brain, can live a long time. A lot of ME/CFS symptoms could be associated with endothelial cell dysfunction, and there have been some preliminary studies suggesting there is endothelial cell dysfunction and perturbation of calcium channels. So, I thought this paper was useful to provide some background.

 

[Amw66]

It seems that this disruption of cell's calcium processes is common in viruses.


A recent SARS-CoV-2 study noted that the virus affects calcium signalling in endothelial cells. Endothelial cells, especially in the muscles and brain, can live a long time. A lot of ME/CFS symptoms could be associated with endothelial cell dysfunction, and there have been some preliminary studies suggesting there is endothelial cell dysfunction and perturbation of calcium channels. So, I thought this paper was useful to provide some background.

Does this link to the calcium ion channel irregularities suggested by the Australian team ( Griffith ?)

 

[Hutan]

Does this link to the calcium ion channel irregularities suggested by the Australian team ( Griffith ?)

It might. The paper goes through the various calcium channels and pumps. Transient Receptor Potential (TRP) channels are one sort of channel.

5.1. TRP Channels
The TRP channel is a non-selective cation channel predominately permeable for Ca2+ [49,50]. It is divided into six sub-families according to their amino acid sequence: TRP canonical or classical (TRPC), TRP vanilloid (TRPV), TRP melastatin (TRPM), TRP ankyrin (TRPA), TRP polycystin (TRPP), and TRP mucolipin (TRPML) [50]. They are ubiquitously expressed in different tissues and cell types and are a key player in the regulation of intracellular calcium. Nevertheless, reports about virus control TRP channels are not numerous.