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Contents contributed and discussions participated by laceemarie

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laceemarie

Targeting therapeutics to an exposed and conserved binding element of the HIV-1 fusion ... - 10 views

www.ncbi.nlm.nih.gov/...PMC154290

shared by laceemarie on 18 Nov 14 - No Cached
  • We report that the C-terminal region of the HIV-1 gp41 ectodomain (and gp160 precursor molecule) appears to be partially exposed and vulnerable to an antiviral agent before the receptor-mediated conformational changes that initiate membrane fusion.
    • laceemarie
      laceemarie on 18 Nov 14
       
      How long is this domain "exposed and vulnerable" before the membranes fuse? Would whatever antiviral treatment that targets this have to be able to hang around, so to speak, for a while in between HIV-host interactions, without being degraded or absorbed or moved to another place in or out of the body?
laceemarie

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

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

shared by laceemarie on 09 Nov 14 - No Cached
  • Humans have 7 APOBEC3 genes and determining how each specifically functions to inhibit retroviruses like HIV is complicated, because all 7 can be produced in a given cell type or tissue.
    • laceemarie
      laceemarie on 14 Nov 14
       
      What cell/tissue type(s) are these APOBEC3 genes naturally turned on in? 
  • To overcome this limitation, we made transgenic mice that express two of the human proteins, APOBEC3A and APOBEC3G in mice that do not express their own APOBEC3. These mice were able to effectively block infection by several mouse retroviruses
    • laceemarie
      laceemarie on 14 Nov 14
       
      What cell type(s) did they use? Does it matter which?
  • We were unable to perform similar assays with in vivo produced MMTV, because the only cell-free virus in mice is found in milk and mammary tumors and we have not yet established breeding colonies of virus-infected human A3 transgenic mice.
    • laceemarie
      laceemarie on 14 Nov 14
       
      Was this a screw up, or is it not that important to look at assays with in vivo produced MMTV. And by "not yet," does that mean they are going to? I feel like if your going to use this virus in your experimental studies, you should figure out ways to perform the assays, regardless of how you get the virus. It would appear that they knew this information before hand, so maybe an assay on MMTV is less relevant. 
    • laceemarie
      laceemarie on 14 Nov 14
       
      *you're
  • ...1 more annotation...
  • Two A3A and A3G mouse strains each were generated, expressing levels of these proteins within the range or at levels lower than that seen in human cells. This likely has relevance to what occurs in individual humans, where non-coding region polymorphisms in A3 genes alter expression levels and may influence progression to HIV-induced disease
    • laceemarie
      laceemarie on 14 Nov 14
       
      Could this have something to do with how HIV works in the HIV controllers? Where they still exhibit virus particles, but at a lower amount, don't necessarily spread the virus as much, and don't exhibit as intense of HIV symptoms?
laceemarie

The Major Genetic Determinants of HIV-1 Control Affect HLA Class I Peptide Presentation - 11 views

www.ncbi.nlm.nih.gov/...PMC3235490

shared by laceemarie on 14 Nov 14 - No Cached
  • Yet a small number of people demonstrate sustained ability to control HIV replication without therapy. Such individuals, referred to as HIV controllers, typically maintain stable CD4+ cell counts, do not develop clinical disease, and are less likely to transmit HIV to others (2).
    • laceemarie
      laceemarie on 14 Nov 14
       
      This is really cool! I have not heard of this until now. Have these people been studied to find out why this occurs? Is it because of the genetics of the person or a certain mutation in the virus? And the key words here are "less likely." That's a pretty broad statement - "less likely" meaning how likely?
laceemarie

Inhibitory activity of dioxolane purine analogs on wild-type and lamivudine-r... - 5 views

onlinelibrary.wiley.com/...pdf

shared by laceemarie on 14 Nov 14 - No Cached
  • laceemarie on 14 Nov 14
     
    Focus paper for November 21!
laceemarie

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

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

shared by laceemarie on 03 Nov 14 - No Cached
  • RABV enters the peripheral nervous system and undergoes long-distance transport arriving at the cell soma and subsequently the CNS [6]. As peripheral neurons are highly polarized cells with long axons, active intracellular transport is vital to the maintenance of neuronal function and survival [7], [8]
    • laceemarie
      laceemarie on 07 Nov 14
       
      As RABV is travelling along the axons, does it interfere with the nerve signals that are also travelling there? I know that rabies results in quite a few neurological symptoms, but do these occur when the virus reaches the central nervous system (ultimately the brain) or as soon as RABV enters an axon of the PNS?
laceemarie

Virus-Mediated Compartmentalization of the Host Translational Machinery - 22 views

mbio.asm.org/...e01463-14.full

shared by laceemarie on 27 Oct 14 - No Cached
  • We further show that the nonstructural protein σNS strongly colocalizes and immunoprecipitates with two proteins in the 43S preinitiation complex (PIC), eIF3A and pS6R, suggesting a role for σNS in the recruitment or maintenance of ribosomes within VF.
    • laceemarie
      laceemarie on 31 Oct 14
       
      If σNS is involved in ribosome recruitment and/or maintenance, this seems like a good target for an antiviral therapy. 
  • This model implies that newly synthesized viral proteins must, by some mechanism(s), be trafficked back into the factory to participate in replication and assembly. Data supporting this model are limited.
    • laceemarie
      laceemarie on 31 Oct 14
       
      "Limited," but still exists. So under what circumstances did/could this happen? Could it be a possible way to avoid an antiviral drug that inhibits σNS?
laceemarie

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

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

shared by laceemarie on 15 Oct 14 - No Cached
  • The fundamental question is the identity of the mechanism by which a vigorously replicating virus, on entry into the body, is silenced in neurons harboring latent virus.
    • laceemarie
      laceemarie on 17 Oct 14
       
      Just to make sure that I understand this, once the virus enters the body, it quickly replicates and all the new virus particles find a nerve cell to infect and once there, the virus is able to sit in silence, so to speak?
  • Thus, VP16, a virion protein brought into the cells during infection, recruits several cellular proteins, including LSD1, to derepress α gene promoters
    • laceemarie
      laceemarie on 17 Oct 14
       
      VP16, a virion protein and a recruiter - this protein sounds pretty important to me. Is there a way or has there been work done with this protein to not allow the derepression at this checkpoint? Is it possible to keep a virus in latency because of alpha gene promoters not getting derepressed so as to not allow the virus to infect the host? I'm not sure if that's a reasonable antiviral therapy or not.
  • In some neurons, the virus establishes a latent, silent state. In other neurons, the virus replicates, and it is most likely that the virus in these neurons is transmitted and replicates in other ganglionic cells.
    • laceemarie
      laceemarie on 17 Oct 14
       
      Is this a random event or does this have something to do with the environment of the neuron? I would assume that specific, different environments would be ideal for each.
laceemarie

An Inquiry into the Molecular Basis of HSV Latency and Reactivation - Annual Review of ... - 3 views

www.annualreviews.org/...annurev-micro-092412-155654

shared by laceemarie on 15 Oct 14 - No Cached
  • Primary HSV infection of the eye results in herpes simplex keratoconjunctivitis with latency established in the trigeminal nerve.
    • laceemarie
      laceemarie on 17 Oct 14
       
      I was wondering why the primary lit paper was doing there tests in corneal cells. I forgot that there is an HSV that infects the eyes.  What exactly happens to the host cell once the virus is derepressed after latency? I'm sure it has said it in one or both of that papers, but I'm confused by the mechanism. The virus doesn't kill the host cell does it? Being that it resides in nerve cells (which is something new to me) and nerve cells don't replicate, killing the nerve seems like a bad idea for them and for us. Does the presence of the active virus (not latent virus) affect the function of the nerve? As in, does the herpes simplex keratoconjunctivitis affect the trigeminal nerve in that the virus interferes with the transmitting of sensory information from the face to the brain?
    • laceemarie
      laceemarie on 17 Oct 14
       
      *Their tests
  • Notably, antibodies to HSV can routinely be detected in the cerebrospinal fluid of otherwise healthy individuals, implying that HSV can establish latency in the central nervous system and cause an adaptive immune response, as noted above by PCR data (24). It is unlikely that antibodies to HSV are passively transported across the intact blood-brain barrier.
    • laceemarie
      laceemarie on 17 Oct 14
       
      If antibodies can be found in the CSF, then HSV can be found in the CSF, right? Does or could HSV use the CSF as as way to travel to other tissues/nerve cellls?
laceemarie

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

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

shared by laceemarie on 12 Sep 14 - No Cached
  • Mass spectrometry was used to identify proteins present within the samples with a minimum of 2 unique peptides and >90% identification probability
    • laceemarie
      laceemarie on 16 Sep 14
       
      I'm confused as to how exactly mass spectrometry was used in this experiment. If the proteins are already separated by molecular weight after the SDS-PAGE, what precisely are they looking for when running a mass spec? It article says, ".... a minimum of 2 unique peptides and >90% identification probability," but this doesn't mean much to me. I understand the identification part because based on the way the molecule splits after being shot with ions, you can get a basic idea of the structure of the molecule. My question with the 2 unique peptides is that each amino acid has a different molecular weight right? So if the proteins were all the same except at the 2 unique peptides, the mass spec would show a different mass to charge ratio for each protein with the varying peptides correct? Would the charge of the amino acids in the peptide have anything to do with the charge portion of the mass to charge ratio? I hope this question came out okay. 
laceemarie

Airborne Transmission of Influenza A/H5N1 Virus Between Ferrets - 12 views

www.sciencemag.org/...1534.full

shared by laceemarie on 04 Dec 12 - No Cached
  • the factors that determine airborne transmission of influenza viruses among mammals, a trait necessary for a virus to become pandemic, have remained largely unknown (18–21)
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