19 thoughts on “Virology lecture #2: The infectious cycle”

  1. so many different methods surprise me, I'd expected one to become dominant and
    outcompete the others

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  3. Wow. Thanks for posting these lectures, I really enjoy them. I think that your “Adenovirus type 5” slide showing the eclipse vs. latent period (I never knew the difference) is actually a multiple-cycle curve since it shows exponential growth of virus. If it was a one-step curve shouldn't it be linear growth?

  4. it stopped with my AOL-browser after 17min , but it worked now with firefox

    It was well understandable for me as nonnative English speaker although you spoke
    quickly.Graphics also good.Captions would be useful. Internet is better than
    real lessons since you can switch back and hear again when you didn't understand
    something and you can make pauses for email,eating,telefone,chatting,dicussing.
    Of cause, with books you can do that too but students
    are maybe not so motivated to read books ?!?

    There are so many different viruses with entirely different mechanisms,
    and thus -presumably- quite different encodings, which are hard to achieve by mutations.

    some enter without receptor
    some don't use translation
    some replicate in 20min (polio:8h)
    some don't need the nucleus
    E.g. why “bud” like flu when you can just burst the cell like polio ?
    Get into the cell, replicate,get out. There should be one optimal way
    to perform this, not dozends ?!

    I learned everything about virology by starting with the sequences(flu).
    I was really surprised when I first saw the anatomy of the
    virus, how complicated it was with these few nucleotides.

    Why do bacteria replicate so much faster ? Because they
    can eat and divide directly and need no host ?
    They need more nucleotides to perform this and thus are larger ?

    Will we one day kill all viruses ?
    Will military/terrorists one day make more dangerous artificial viruses ?

  5. well, it's “CPE= cytopathic effect” (==>burst(polio)) in the course,
    in the paper they say “lytic” virusus (–>lysis),
    wikipedia says “apoptosis”

  6. I liked these lectures too. I'm going to remember to start any virus replication explanation with polioviruses. Positive RNA viruses are the best place to start when you are discussing the virus replication.

  7. what's the advantage of being negative ?
    can it switch polarity by evolution ?
    are there viruses with both variants (which reassort…)

  8. For this lecture I have the following questions;
    Does the use of Phenol Red not have effects to living cells? As Phenol red is linked to renal failure, can theuse of Phenol red affect the living cells used in culture or the virus entities themselves?
    Do the plastic petri dishes contain Bisphenol A and are they emitting toxic agents to the living cells or to the virus entities? All of this from the benevolent petroluem industry?
    Was vaccination also the start of autoimmune disease in animals and humans?

  9. One can talk about the advantages of being negative or the disadvantages of being positive. If one's positive, the virus (anthropomorphizing) has to choose between replication or protein production. By being negative, the virus can do both.

    I think with the high rate of virus mutation, it's hard to say which of the different categories of RNA viruses came first.

    Are you talking about ambisense viruses which are technically negative strand but also can act as positive strand?

    Also, to a comment above, I like working with viruses because they contain so much with so little. Because of this, they serve as good models (pathogen/host) and possibilities in reprogramming (if you think of genes as java classes, you could potentially have the basis for biological programming).

  10. not talking about ambisene. Just wondering why there are different senses and whether
    viruses can flexibly switch.
    (same for RNA-DNA, budding vs. bursting the cell, envelope or not,…)
    Also to your reprogramming strategies … it's interesting how “genetical algorithms”
    are implemented with mutations in nature. But our designed computer-algorithms
    look superior, so there should be space for improvement
    through artificial algorithm-design , so will we see man-made re-programmed “improved” viruses
    soon ? And then the military and terrorists will get it …

  11. When I last read a book on virology, it stated that while some virions were destroyen in low pH, all known viruses could be destroyed by high pH. Is this still true? Is this a significant effect? Would using real soap rather than pH 5.5 soaps help avoid hospital outbreaks of norovirus? How does petrol destroy virions?

    Sorry if this is a tad confused. Thanks again for a great lecture, and thanks for making it downloadable so I'm encouraged to listen to it again to see whether that clarifies things.

  12. Wonderful Lecture! Do the amyloid fibrils as mentioned in previous post with regards to XMRV/HIV increase the P(k) ?

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