In Bangladesh, Nipah virus is spread from Bats to human and from primary human cases to secondary human cases. In Malaysia, Nipah virus is spread from Bats to pigs to people, where it cannot transmit forward (humans are a dead end). What is main reason for the difference between Nipah virus transmission in these two locations?

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Hubert KochLv2

25 Jun 2018

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Read the following passage focusing your attention on the scientific procedures and scientific abilities illustrated in it. Think about what types of experiments (observation, testing or application) are described. Identify the hypothesis, predictions, outcomes of experiments and assumptions that appear in the passage. The standard explanation of how humans originally acquired AIDS is that HIV (human immunodeficiency virus) originally was transmitted to humans from monkeys or apes carrying SIV, simian immunodeficiency virus. How could the transmission have occurred? Several similar hypotheses involve an African hunter coming in contact with monkey blood. For example this could have occurred when a hunter butchering a monkey, got some of its blood in a cut, or when a human ate undercooked monkey meat, or when a monkey bit a human. Depending on one's assessment of the genetic diversity of HIV over time, this transmission might have occurred only a few decades ago or, alternatively, hundreds or thousands of years ago. If the latter is correct then AIDS could have been restricted to remote African villages until recent decades when trade and international travel led to the current pandemic. There are however other alternative explanations for the spread of AIDS. One of them is that AIDS arose from contaminated polio vaccines used in Africa from 1957-59. Why is this a plausible explanation? Polio vaccines are cultured on apesâ kidneys, so contamination of a batch of vaccine by an SIV is a possibility. There is a precedent: in the 1950s and early 1960s millions of doses of polio vaccine were contaminated by another simian virus, SV-40. The vaccine alleged to be the origin of AIDS was given to hundreds of thousands of people in central and west Africa from 1957-1959. These locations later had some of the world's highest levels of HIV infection. The timing is also right, since the earliest known cases of AIDS date from the 1960s; the earliest HIV-positive blood sample was collected in Kinshasa in 1959. At the time, there was no way of testing for the presence of SIVs, which were only discovered in the 1980s. Another factor adds plausibility to the theory: the vaccine was given to many infants less than a month old, in an extra high dose. Since the immune systems of infants are not fully developed, this is an excellent way to help a virus jump the species barrier. Some scientists argue that the above explanation is not necessarily correct but that it is worth taking seriously. There are a number of ways to test it. One is to analyze stocks of polio vaccine; if the explanation is correct, then it is probable that some of the vaccines will carry SIV. Another is to scrutinize records of early polio vaccination campaigns in Africa. If it is true that the immunodeficiency virus passed to humans by way of those vaccines, the areas where the campaigns took place would be the same as those where the initial sprouts of the disease occurred and where the larger number of cases occurred during the early stages of the pandemic. Another is to analyze blood samples in Africa from the 1950s and earlier (pre polio vaccination): if the immunodeficiency virus was transmitted via the polio vaccine, HIV should not be found. Adapted from âPolitical refutation of a scientific theory: the case of polio vaccines and the origin of AIDSâ. Brian Martin, published in Health Care Analysis, Vol. 6, 1998, pp. 175-179. Now reread the passage and answer the following questions.

5. For each experiment, write an outcome that would disprove the hypothesis of AIDS passing from monkeys to humans through polio vaccines.

6. What outcomes of the experiments would fail to disprove the hypothesis of AIDS passing from monkeys to humans through polio vaccines?explain.

7.What outcomes would prove the hypothesis? Hint: This is not the same as question 6. Think about what would you need to do to 100% prove a hypothesis.

8. For what reasons do scientists need to conduct testing experiments?

ochrejackal75

1. Unlike Ebola virus, SARS virus
a. has large spikes that look like a âcrownâ.
b. is enveloped.
c. is helical.
d. is in the family Togaviridae.
e. is a ssRNA virus.

2. Which virus or virus family is described in the followingpassage?
Electron micrographs of the hemagglutinin subunits (in the presenceof SDS) showed
rods approximately 40 Ã wide and 140 Ã long. The neuraminidasesubunits had a quite
different appearance. In the presence of SDS, these were seen asoblong structures about 85 Ã long and 50 Ã wide with a centrallyattached fibre 100 Ã long possessing what appeared to be a diffusetail or small knob about 40 Ã in diameter at its end.1
a. Togaviridae
b. Epstein-Barr virus
c. Smallpox virus
d. Orthomyxoviridae
e. Filoviridae
f. Rabies virus

3-Following is a passage from the New England Journal ofMedicine:
______________________ is an exclusively human herpesvirus that ...becomes latent in
cranial-nerve and dorsal-root ganglia, and frequently reactivatesdecades later to produce shingles and postherpetic neuralgia. Inimmunocompetent elderly persons or
immunocompromised patients, ____________________ may producedisease of the central nervous system.
This passage refers to which virus?
a. West Nile virus
b. Smallpox virus
c. Epstein-Barr virus
d. Ebola virus
e. Varicella-zoster virus

4. Pneumoviruses can cause colds and pneumonia in humans. They aresingle-stranded,
negative-sense, nonsegmented RNA viruses. These enveloped virusesare surrounded by an envelope that is characterized by fusionglycoproteins and host-derived proteins. With this knowledge, it islikely that pneumoviruses
a. enter host cells via endocytosis.
b. leave host cells by budding.
c. enter host cells via membrane fusion.
d. A and B
e. B and C

5. Recall that poliovirus is a positive-sense (+) ssRNA virus. The5â Ã ? 3â strand of RNA,
once uncoating has taken place, can serve as an mRNA and encode forviral proteins.
However, in order for the virus to create more +ssRNA to package indaughter viruses, it must
a. generate a dsRNA molecule that can encode for the synthesis ofmore +RNA.
b. integrate into the host cell DNA.
c. utilize an RNA-dependent DNA polymerase to make aheteroduplex.
d. undergo reassortment
e. All of the above

6. Some influenza hosts, such as humans and pigs, cansimultaneously contract human,
avian and swine influenza viruses at the same time. What can occurduring the maturation phase of virus replication in such ahost?
a. Reassortment
b. RNA of all three sources: human, swine and avian, can bepackaged into a single
virion.
c. Genetic shift
d. All of the above

7. The HIV virion contains enzymes/proteins that do all of thefollowing EXCEPT
a. An enzyme that creates âDNA using +RNA as template.
b. A protein that serves as a chemokine receptor.
c. A DNA-dependent DNA polymerase.
d. An enzyme that allows +/- viral DNA to be spliced into the hostcellâs DNA.
e. A protein that mediates membrane fusion.

8. After a long series of biochemical tests, Kyle and Matt werefinally able to identify their Gram-negative unknowns asPseudomonas aeruginosa and Shigella dysenteriae,
respectively. As they compare notes, they realize that theirunknowns are in the
___________ Pseudomonadaceae and Enterobacteriaceae, respectively.However, they also note that both of their unknowns are in the______________ ? proteobacteria.
a. genera, species
b. phyla, family
c. families, class
d. order, phyla
e. classes, order

9-Hydrogenobaculum acidophilum is a resident of YellowstoneâsNorris Geyser basin. This thermoacidophilic microbe grows instringy, white mats and is a member of the phylum Aquificae.Hydrogenobaculum acidophilum
a. could be further researched in Volume 2 of Bergeyâs Manual ofSystematic
Bacteriology.
b. is in the domain Archaea.
c. is a deeply branching bacterium.
d. is a proteobacterium.
e. All of the above

10-After talking about the Group A Streptococci (GAS) and theircapability to sometimes cause a flesh-eating disease callednecrotizing fasciitis, Derek decides to research this group a bitmore. As he reads, he quickly learns that
a. they are microaerophilic Gram-negative rods.
b. they are in the phylum ?-proteobacteria.
c. they are found Volume 4 of Bergeyâs Manual of SystematicBacteriology.
d. they have less than 50 mol % GC content.
e. none of the above

I have recently peformed an ELISA (Enzyme-linked immunosorbentassay), but I still have some questions, let me first outline whatI did:

We had a number (20) of tubes containing fake 'bodily fluids' ,namely saliva. One of these tubes contained the Epstein-Barr virus,which on its turn causes Pfeiffer's disease, aka the 'kissingdisease' (so we basically conducted an experiment to see how fastthe virus would spread within a class if everybody started kissingeach other, if you don't mind the crudity).
Everybody mixed their saliva with the saliva of 3 other people,so at the end everybody had a tube with the saliva of 4 differentpeople in it.
Since we worked in pairs of 2, every duo got a microtiter platewith 12 wells in it: 3 wells for a positive control, 3 wells for anegative control, 3 wells for the fluids of 1 of the duo and 3wells for the fluids of the other one. You pippete in (is thatcorrect?) the fluids accordingly.
After a while you rinse and clean the wells with washbuffer.
Then you pippete in the primary antibody in each well.
After a while you rinse and clean the wells with washbuffer.
Following this you pippete in the secondary antibody (conjugatedwith the enzyme HRP).
After a while you rinse and clean the wells with washbuffer.
Finally, you add the enzyme substrate (TMB) to each well. Thiscauses a blue color if when in contact with HRP. The positivecontrols must come out blue, the negative must come out colorless,and the other wells can go either way, depending if you have thevirus.

I hope this is not to crudely explained, again. These are myquestions concerning the experiment:

What do the components of the acronym 'ELISA' actually standfor? Does immunosorbent refer to the binding of the antigens to thewells? My English isn't too good, and these acronyms andabbreviations often seem foreign to me (nevermind that they areforeign since I'm not English, you get the point I hope).
When you pippete in the saliva in the wells, what actuallysticks to the wells? All of the antigens in your saliva? Becauseit's hard to believe that they make special microtiter plates forevery single antigen seperately. I assume it is only the antigens,since the primary antibodies attach to the antigens only, so thereis no need for the microtiter plate itself to bind toantibodies.
How would we get the primary and secondary antibody? This is myassumption: The primary antibody we get is by injecting someantigens of the Epstein-Barr Virus into a human and then taking aserum. The secondary antibody could be gotten by injecting a randomhuman primary antibody into ANY animal, irrelevant which anyimal,and then taking a serum. After that you conjugate an enzyme to thesecondary antibody. Is this correct?