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slgoogin8981

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

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

shared by slgoogin8981 on 15 Oct 14 - No Cached
  • R111 recombinant is not reactivation-defective because it is able to reactivate in the presence of inhibitors of protein synthesis in the same manner as the WT parent virus, and (b) because the only significant difference in the WT and R111 viruses is the presence of the REST gene in the latter virus, the data suggest that expression of this gene blocks reactivation and that suppression of protein synthesis, including that of REST, enables reactivation.
    • becky214
      becky214 on 16 Oct 14
       
      I am confused about when REST blocks reactivation and when it enables it. It says the gene blocks reactivation but continues to say it enables it. Does REST only enable reactivation if it plays a role in suppressing protein synthesis?
  • with dexamethasone or dexamethasone and cycloheximide
  • Specifically, a stress response generated by virus entry recruits or activates REST to enable the assembly of the HCLR complex. Stress responses have been postulated to activate REST
    • becky214
      becky214 on 16 Oct 14
       
      I think this is interesting because REST is not usually found in neurons. I'm curious as to how the neuron recruits this gene. Does the virus actually recruit it? Or is it just a cellular response to the stress of viral entry? 
  • ...13 more annotations...
  • HSV takes advantage of the neuronal stress response to enter into a silent, latent state. To assist in the execution of this plan, HSV evolved a DNA sequence that allows itself to be suppressed in neurons and a mechanism to maintain an equilibrium between total suppression and potential to exit from the latent state.
  • translocated from satellite cells
  • 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.
  • Finally, in contrast to the events following entry of virus after retrograde transport from the periphery, the data suggest that reactivation does not trigger a stress response that leads to activation of REST
    • alexridesducati
      alexridesducati on 17 Oct 14
       
      Has anyone been able to pinpoint the exact step in infection that activates REST so that it can be studied? If so, perhaps it is possible to manipulate the effects of that step in order to induce an artificial response to the reactivation of HSV1 from its latency period in order to retrigger the stress response that leads to REST activation.
  • Thus, VP16, a virion protein brought into the cells during infection, recruits several cellular proteins, including LSD1, to derepress α gene promoters. One α gene product, infected cell protein 0 (ICP0), derepresses β and γ1 genes. Ultimately, the onset of viral DNA synthesis enables the expression of very late, or γ2, genes (4).
    • Sean Hogan
      Sean Hogan on 17 Oct 14
       
      Is this why the latent infection occurs in the ganglia of the PNS? The necessary proteins for gene derepression can't be recruited in the CNS or other cells?
  • In contrast, simultaneous expression of all viral genes during reactivation from latency is likely to minimize yield, but the mission of the virus is to assemble enough viruses to reach the portal of egress from the body (e.g., mouth, genitals) rather than to overwhelm the host with infectious virus.
    • Sean Hogan
      Sean Hogan on 17 Oct 14
       
      This might be the coolest statement in the whole paper. The discussion above kind of painted a picture of HSV infecting the PNS only but the reason for it's inability to reach the CNS didn't receive as much attention. I think this statement summed it all up though.HSV doesn't care about high virion yields or whether a productive or latent infection is necessary, it just wants to reach the body portals. The virus is "smart," enough to avoid the CNS and keep it's host alive.
  • Between 5 and 24 h after excision, mRNAs representative of all viral gene kinetic groups increase 100-fold in amount. Viral DNA also increases in amount, indicating that viral proteins are made. At the same time, viral LAT and miRNA concentrations decrease at least 10-fold (34). It is convenient to define the initial phase lasting no more than 5 h as the preactivation phase and the remaining time interval as the activation phase.
    • rmeloche10
      rmeloche10 on 17 Oct 14
       
      I'm having trouble grasping why the massive disparity between viral DNA and viral LAT. Obviously there would be some disparity when reactivation occurs, but wouldn't the production of more DNA contribute to even a small amount of LAT production and not a minimal 10 fold decrease?
  • 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.
    • nleonard11
      nleonard11 on 20 Oct 14
       
      I thought this process of finding out that the HCLR complex activates from stress was very interesting. Using WT viral genomes appears to be a very effective way to test many virus functions.
    • nleonard11
      nleonard11 on 20 Oct 14
       
      I was just wondering why the virus goes into a latent after 30 days? What exactly is it waiting to do and what conditions need to be present for it to become active again.
    • slgoogin8981
      slgoogin8981 on 19 Nov 14
       
      It would be interesting to know the amount that REST is seen in non-neural cells and nerve cells in the absents of HSV-1. I was state earlier that REST is not normally found in never cells.
Trevor F

Unique molecular signatures of disease brain endothelia provide a novel site for CNS-di... - 5 views

www.ncbi.nlm.nih.gov/...PMC3181494

Adeno-associated virus gene therapy

shared by Trevor F on 27 Sep 12 - No Cached
  • Trevor F on 27 Sep 12
     
    Great paper for introductory look at adapting adeno-associated viruses (AAV) to different cell tropisms.  Although the scope of this article is the CNS, and more specifically the brain.  Also goes over how brain vasculature expresses different characteristics in disease states that allows for specification of AAVs to have tropism for the diseased epithelial beds.
Casey Finnerty

HIV Latency - 0 views

perspectivesinmedicine.org/...a007096.full

virology microbiology HIV latency

shared by Casey Finnerty on 29 Oct 12 - No Cached
  • For HIV-1, the term latency was initially used in the clinical sense to describe the long asymptomatic period between initial infection and the development of AIDS. However, with the advent of sensitive RT-PCR assays for viremia (Piatak et al. 1993), it became clear that HIV-1 replicates actively throughout the course of the infection, even during the asymptomatic period. The major mechanism by which HIV-1 evades immune responses is not latency but rather through rapid evolution of escape mutations that abrogate recognition by neutralizing antibodies and cytolytic T lymphocytes (Bailey et al. 2004). Nevertheless, it has become clear that HIV-1 can establish a state of latent infection at the level of individual T cells
Casey Finnerty

Fish diseases: Viral Hemorrhagic Septicemia: Minnesota DNR - 0 views

www.dnr.state.mn.us/...vhs.html

VHS virology

shared by Casey Finnerty on 29 Aug 12 - No Cached
  • A Cornell University research team’s recent finding of traces of the Viral Hemorrhagic Septicemia virus (VHS) in fish inhabiting Wisconsin and Michigan waters of Lake Superior
  • So far the virus has not been detected in the inland waters of Minnesota.
  • If you would like to find out the most recent VHS infected sites call the DNR Pathology Lab at 651-259-5096.
Casey Finnerty

Powassan Virus (POW) Basics - Minnesota Dept. of Health - 0 views

www.health.state.mn.us/...basics.html

Powassan minnesota virology

shared by Casey Finnerty on 29 Aug 12 - No Cached
  • Initial laboratory testing in 2009-2010 found blacklegged ticks infected with POW virus in parts of north-central, east-central, and southeastern Minnesota, areas highly endemic for other tick-borne diseases such as Lyme disease.
Casey Finnerty

First Death in Minnesota from Powassan Virus - 0 views

www.winonadailynews.com/...99-11e0-89ab-001cc4c03286.html

Powassan virology

shared by Casey Finnerty on 29 Aug 12 - No Cached
  • Locally, Powassan infected ticks have been found in Houston County
Casey Finnerty

Panel Recommends HPV Vaccine for Boys and Young Men - NYTimes.com - 0 views

www.nytimes.com/...26vaccine.html

microbiology HPV vaccination virology

shared by Casey Finnerty on 29 Aug 12 - No Cached
  • HPV infection is the most common sexually transmitted disease — between 75 percent and 80 percent of females and males in the United States will be infected at some point in their lives. Most will overcome the infection with no ill effects. But in some people, infections lead to cellular changes that cause warts or cancer, including cervical, vaginal and vulvar cancers in women and anal cancers in men and women. A growing body of evidence suggests that HPV also causes throat cancers in men and women as a result of oral sex. HPV infections cause about 15,000 cancers in women and 7,000 cancers in men each year. And while cervical cancer rates have plunged over the past four decades because of widespread screening, anal cancer rates in men and women have been increasing. Head and neck cancers have also been increasing, with the share associated with HPV infection increasing rapidly — perhaps because oral sex has increased in popularity.
Casey Finnerty

PLoS ONE: Fatal Cases of Influenza A in Childhood - 7 views

www.plosone.org/...10.1371%2Fjournal.pone.0007671

shared by Casey Finnerty on 10 Sep 12 - No Cached
  • This work presents a rare insight into fatal influenza H3N2 in healthy children.
    • Casey Finnerty
      Casey Finnerty on 10 Sep 12
       
      So I think we can see why some virologists were uncomfortable with keeping the swine barn open at the state fair this year!
  • Tyrell Varner on 10 Sep 12
     
    Vaccinations are nice, until an antigenic strain is formed. In which case it's back to the drawing board to create a new one as soon as possible. Influenza is constantly changing in order to thrive. Amazing!
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