Virus Cell to Cell Transmission

[kiwibird]

https://jvi.asm.org/content/84/17/8360

Virus Cell-to-Cell Transmission

Walther Mothes, Nathan M. Sherer, Jing Jin, Peng Zhong

However, spread by direct cell-cell contact is likely more than a salvage pathway for the unfit. While researchers were forced to discover the importance of cell-to-cell spread for viruses with poor infectivity-to-particle ratios, it is worthwhile to consider the possibility that even the most stable viruses use cell-to-cell spread. There are several appealing advantages associated with direct cell-to-cell spread that could be exploited by many viruses. The first is speed: rather by going through all the steps of cell-free transmission, the entire extracellular replication cycle of release, transmission, and entry can proceed quickly at sites of cell-cell contact and exploit cytoskeletal forces for the purpose of spreading. Moreover, the observed enhancement of budding at sites of cell-cell contact can promote spreading at lower levels of gene expression (56). The second is immune evasion: limited exposure time to the extracellular space can allow evasion of neutralizing antibodies (39, 51). Third, exploiting cell-cell communication is an effective way to overcome the various physical and immunological barriers within an organism in order to spread the infection......

Consequently, viruses end up “surfing” toward endocytic hot spots at the cell body (17, 68-70, 110, 115). As such, viruses do not recruit an individual myosin motor to each particle but, rather, utilize the general turnover of F-actin. Thus, viruses engage a high-affinity interaction with receptor-expressing cells that allows them to utilize actin-driven motion to move toward target cells (17, 111, 112) (Fig. 2B).

https://link.springer.com/article/10.1007/BF01188423

Co-localization of the myelin-associated glycoprotein and the microfilament components, F-actin and spectrin, in Schwann cells of myelinated nerve fibres

https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1000519

Theiler's virus offers a remarkable example of a pathogen that navigates the various cells of the organism to evade immune responses and establish a persistent infection. Here, we discuss the transition from neuron to myelin and oligodendrocyte infection, a step that is crucial for the persistence of this virus in the central nervous system (CNS).

Interesting articles about the mode of transport of enveloped virus (in the first article HIV), intracellular (avoiding antibodies), extra cellular and via nerve cells (also avoiding the extra cellular range of defences).

 

[JJackson]

Kiwibird
Syncytia is also a feature of SARS-CoV-2. The image below is taken from https://www.embopress.org/doi/full/1...mbj.2020106267

 

[gsgs]

with only one virus generation every 6 hours and >10000 (100000?) viruses per cell they can't do much harm with cell-to-cell trveling

 

[kiwibird]

https://flutrackers.com/forum/forum...l-inoculation-of-sars-cov-2-in-k18-hace2-mice

I was wondering if it was more of a problem with the problems involving they delamination of the myelin sheath that was reported - also the nerve and brain problems - especially of long covid. The encephalitis in Tetanos post above caused 100% mortality! Not just catching the virus that is the problem - it is what is affected - perhaps what route of infection it takes inside the body. What is strange about this virus is the way it affects people differently. Married couples having the same symptoms and whole families being severely affected while other couples have one person suffering badly while the other seems almost asymptomatic. In at least some cases it must be environmental/epigenetic.

 

[JJackson]

You may find this of interest. https://www.microbe.tv/twin/twin-5/
I think it was this episode in which they discussed the route into the CNS via the olfactory bulb and the various barriers it would face.
I suspect, without direct evidence, that a lot of the variability in patient symptoms will turn out to be determined by the variation in host genetics and random chance (I would include gene expression control by epigentetics). Environmental factors in families like shared nutritionally poor diet should also play a part.
This link may be helpful regarding immunotypes associated severe COVID.
https://www.microbe.tv/immune/immune-33/