A high particle-to-pfu ratio is sometimes caused by the presence of noninfectious particles with genomes that harbor lethal mutations or that have been damaged during growth or purification. Another explanation is that although all viruses in a preparation are in fact capable of initiating infection, not all of them succeed because of the complexity of the infectious cycle. Failure at any one step in the cycle prevents completion.
A high particle-to-pfu ratio does not indicate that most particles are defective, but that they failed to complete the infection.
Inosine-containing RNA is a novel innate immune recognition element | MicrobiologyBytes - 0 views
Are all virus particles infectious? - 0 views
'Binding, bending and bonding': polypurine tract-primed initiation of plus-strand DNA s... - 0 views
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This review describes nicely HIV replication and the role of the PPTs.
No Video. No Photos. No Names. Inside New York's Ebola Monitoring Operation. - NYTimes.com - 0 views
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This article gives a very good description of the size of the Ebola monitoring effort underway in NYC and around the country.
MSF Protocols for Staff Returning from Ebola-Affected Countries | MSF USA - 0 views
Discussion Ebola Research Needs | Video | C-SPAN.org - 2 views
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This panel has the best overview of the research needs for Ebola virus that I have seen. It includes the presentation by CJ Peters that I discussed in class.
Viruses as a Cure - NYTimes.com - 0 views
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When they prevented germ-free mice from making a receptor on the surface of their cells, infection with norovirus didn’t lead to an improvement in their guts.That receptor only latches onto one type of molecule. It’s called Type 1 interferon, and it’s produced by cells when they’re invaded by viruses.
CRISPR mediated resistance to bacteriophages in prokaryotes - 11 views
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journal article for 11/21 / 12/1
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We may need another link to this paper because the link leads to a page that is telling me I cant view the entire paper, just the abstract. -
There is an option to scroll through the pages of the article (the shaded border with an arrow on it)
Targeting therapeutics to an exposed and conserved binding element of the HIV-1 fusion ... - 10 views
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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.
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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?
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and those that can eliminate infected cells, thereby reducing persistent and latent reservoirs of the virus.
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It would be interesting to see if there will be a drug that can eventually do this that will be low-cost and is manageable in dosage. The problem is how much the virus mutates to evade these drugs and the host immune system. Combination therapy with the RT inhibitor, protease inhibitor, the experimental design listed her and this drug may be effective at treating HIV in the future.
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These studies do not determine whether 5-Helix interacts with the native conformation of Env or, rather, some misfolded conformation of gp41 and gp160 on the cell surface.
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What would cause the misfolding of Env? Wouldn't it be advantageous to interact with both in order to prevent HIV infection?
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Focus paper for wednesday
The Major Genetic Determinants of HIV-1 Control Affect HLA Class I Peptide Presentation - 2 views
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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
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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?
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The Major Genetic Determinants of HIV-1 Control Affect HLA Class I Peptide Presentation - 11 views
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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).
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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?
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It is interesting to see that there are 3 allelic variants that correlate with disease prognosis, but how does this information benefit society? We can't change peoples genetic so to alter their prognosis. Is this just a benefit to know what medications would be most beneficial with the least amount of side effects?
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Abstract
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Presentation Paper 11/14
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