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Contents contributed and discussions participated by ameliaobert

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ameliaobert

PLOS Pathogens: Different Modes of Retrovirus Restriction by Human APOBEC3A and APOBEC3... - 22 views

www.plospathogens.org/...10.1371%2Fjournal.ppat.1004145

shared by ameliaobert on 09 Nov 14 - No Cached
    • ameliaobert
      ameliaobert on 14 Nov 14
       
      If A3A is less clear, but does not get packaged, where must the A3A involvement with the incoming virus be located (for myeloid cells)? As well as if it is known to use retroelement retotransposition and replication inhibiton in paraoviruses by nh2 to oh independent means, how does the A3A know to be signlle to change the structure of cystine?
ameliaobert

The Major Genetic Determinants of HIV-1 Control Affect HLA Class I Peptide Presentation - 2 views

www.diigo.com/...fbd43783d2e54e9350c549f5f64a1f

shared by ameliaobert on 14 Nov 14 - No Cached
  • The most significant residue, position 97 in the floor of the peptide binding groove of HLA-B, is associated with the extremes of viral load, depending on the expressed amino acid. This residue has been shown to have important conformational properties that affect epitope-contacting residues within the binding groove (26, 30) and has also been implicated in HLA protein folding and cell-surface expression
    • ameliaobert
      ameliaobert on 14 Nov 14
       
      Most Interesting: That one specific residue can produce high results for a virus for comformational changes pertaining to the epitope binding groove. Most Confusing: If for HLA-B this residue position is important, than in HLA-A and HLA-C what residue would be important for the specific binding grove and conformational epitopes? Would 97 be most important or would if not what would be ther reaonsing behind different residues for different HLA?
ameliaobert

Rabies Virus Hijacks and Accelerates the p75NTR Retrograde Axonal Transport Machinery - 14 views

www.ncbi.nlm.nih.gov/...PMC4148448

shared by ameliaobert on 03 Nov 14 - No Cached
  • In neurons, infected cells may mistake RABV particles for cargo and thus recruit trafficking components, allowing viral particles to undergo long-range axonal transport to the neuronal cell body, as was found in the case of adenovirus and the CAR receptor
    • ameliaobert
      ameliaobert on 07 Nov 14
       
      Most confusing: How would a cell "mistake" a virus particle for cargo and then give it direct access to the nucleus? Does it have specific signals radiating from it or receptors that triggers this trafficking component mishap?
  • we suggest that RABV hijacks a specific mechanism that enables the neuron to transport cargos over long distances.
    • ameliaobert
      ameliaobert on 07 Nov 14
       
      To my further question: is this the cellular "mistake" that is happening by the cell that aids in trafficking of this virus? If so interesting that is isn't the cell itself, but the virus taking over a cellular process.
ameliaobert

HSV carrying WT REST establishes latency but reactivates only if the synthesis of REST ... - 7 views

www.pnas.org/...E498.long

shared by ameliaobert on 15 Oct 14 - No Cached
  • The same concentration of HDAC inhibitor was ineffective in inducing the reactivation of R111 recombinant virus in ganglionic organ cultures maintained in medium containing anti-NGF antibody.
    • ameliaobert
      ameliaobert on 18 Oct 14
       
      Interesting: That there is an inhibitor for chromatin remodelling (HDAC). Confusing: Is if HDAC can inhibit properly for WT virus, but not for R111 recombinant, that obtains REST. How does REST make the HDAC inhibitor ineffective ia stressed neuron? I understand that REST is what the DNA can be wrapped about and help with latency, so it that why the HDAC cannot inhibit, since REST is already aiding in latency.
ameliaobert

Norovirus Translation Requires an Interaction between the C Terminus of the Genome-link... - 75 views

www.jbc.org/...21738.long

shared by ameliaobert on 12 Sep 14 - No Cached
  • Importantly, however, despite the interaction between the norovirus VPg protein and eIF4E, it appears to be dispensable for MNV translation initiation, at least in vitro
    • ameliaobert
      ameliaobert on 15 Sep 14
       
      I find it interesting that the MNV is depensable if incorporated in vitro. Im curious as to why this could be.
  • The mutation F123A ablated the ability of VPg to co-purify eIF4G, eIF4A, and PABP but did not affect the ability of NTAP-MNV VPg to co-purify eIF4E (Fig. 5), suggesting that the eIF4E and eIF4G binding regions on VPg are distinct
    • ameliaobert
      ameliaobert on 17 Sep 14
       
      If F123A mutation is observed through data analysis (co-purification) that the eIF4E and eIF4G are distinct, so differ from each other. Then, why does the data suggest that the direct interacts of VPg with eIF4G determines the eIF4F binding capacity from the data obtained? As well as how do these purification datas are able to determine if the binding capacities for the virus VPg proteins are direct interactions?
  • These data would suggest that the direct interaction of VPg with eIF4G largely determines the eIF4F binding capacity of the norovirus VPg protein.
  • ...1 more annotation...
  • some of which function directly in translation initiation, whereas others may contribute to the regulation of host cell translation by virus infection.
    • ameliaobert
      ameliaobert on 17 Sep 14
       
      So here, they are saying that the initiation factors, some directly interact with the viruses translation to mRNA, whereas the other initiation factors present in teh virus contribute there translation factors specifically to when the host cells get involved with the virus translation factors? Basically specifically encoding for specific initiation translation factors based on the area of translation (i.e. from the virus or from the host cell)?
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