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Importantly, we show that SIV Nef is required for optimal replication in primary rhesus macaque astrocytes and that normalizing input virus by particle number rather than by infectivity reveals a disparity between the ability of a Nef-deficient virus and a virus encoding a nonmyristoylated form of Nef to replicate in these central nervous system cells.
33.4 kb -A novel nidovirus was identified in the gastropod mollusk Aplysia californica -The aplysia californica nido-like virus (AcNV) presents a 35.9 kb RNA genome -AcNV has a broad tropism, is enriched in the CNS, and accumulates in neurons -The unique features of A. californica enables single-neuron virus dynamics of AcNV
The gI mutant replicated to normal titres in the oropharynx and could be recovered from the trigeminal ganglia but not from other parts of the central nervous system, suggesting that gI facilitates the spread of the virus from neuron to neuron.
The subsequent distribution of virus in a quantitative sense depends on a complex of interactions between virus and the different cells of the host, rather than solely on the number of virus particles and their rate of translocation.
Moreover, they could evolve much faster by this virus-type strategy than by a primitive cellular organism.
Rabies virus can induce structural neuron damage.
IMPORTANCE Infection of a cell by more than one virus particle implies sharing of cell resources.
This is in contrast to other systems (for example WEE—chick embryo fibroblasts) where virus is released very rapidly and free virus concentration may be considered a reasonable approximation of “total” virus.
In spite of a certain inability of CVS to infect some neuron types, the virus appears relevant to provide new information regarding the complex network of olfactory-related neurons into the CNS.
Such neuron-specific transgenic complementation of recombinant rabies virus holds great promise for obtaining cellular-resolution wiring diagrams of the mammalian CNS.
We identified neuron-to-neuron propagation as one underlying mode of virus spreading in cell culture.
In conclusion, our results indicated that some neurons are resistant to virus-mediated cell death and provide a framework for studying the effects of prior coronavirus infection on neuron function.
One interpretation of this observation is that the productive infection which follows activation of latent virus in the neuron leads to the destruction of that cell.
Thus, Sindbis virus infection of mice provides a model system for studying virus-neuron interactions.
However, it is impossible to distinguish specific effects on the virus-neuron relationship from more general consequences of infection mediated by immune or non-neuronal support cells in live animals.
These data provide a model for studying neuron-virus interactions at the single-cell level as well as via bulk biochemistry and will be advantageous for the study of neurotropic viruses in vitro.

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Dog dies from anti rabies shot
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TRIM21 plays a crucial role in regulating innate immunity by interacting with key proteins involved in antiviral responses. It has been found to negatively regulate the PKR-eIF2α signaling pathway, which is essential for inhibiting viral replication. Additionally, TRIM21 interacts with viral proteins like the SARS-CoV-2 nucleocapsid protein, leading to its ubiquitination and subsequent degradation, thereby inhibiting viral particle assembly and potentially preventing cytokine storm. Moreover, TRIM21 modulates the cGAS/STING pathway, enhances antigen presentation, and activates cytotoxic T cell-mediated antitumor immunity in response to radiation, highlighting its role in antitumor immunity as well. Overall, TRIM21 emerges as a multifaceted regulator of innate immunity with implications for both antiviral defense and antitumor responses.
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