The strategy is to look for unique processes that occur in virus infected cells but not uninfected cells. Look at some of the enzymes encoded by viruses, and the processes they catalyze to find ideas for inhibiting virus replication.Antiviral drug<span>, </span><span>any agent that is used in the </span>treatment<span> of an </span>infectious disease<span> caused by a </span>virus. Viruses are responsible for illnesses such as HIV/AIDS<span>, </span>influenza<span>, </span>herpes simplex<span> type I (cold sores of the mouth) and type II (genital herpes), </span>herpes zoster<span> (shingles), viral </span>hepatitis<span>, </span>encephalitis<span>, infectious </span>mononucleosis<span>, and the </span>common cold<span>.</span>
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<span>Which is not a difference between a population showing exponential growth and a population showing logistic growth?
</span><span>c. carrying capacity </span>
Answer:
62°F (17°C) to -60°F (-51°C) at the tropopause.
Answer:
the answer is A. E. coli B
Explanation:
The multiplicity of infection (MOI) refers to the ratio between the numbers of viruses used to infect <em>E. coli</em> cells and the numbers of these <em>E. coli </em>cells. Benzer carried out several experiments in order to define the gene in regard to function. Benzer observed that <em>E. coli </em>strains with point mutations could be classified into two (2) complementary classes regarding coinfection using the restrictive strain as the host. With regard to his experiments, Benzer observed that rII1 and rII2 mutants (rapid lysis mutants) are complementary when they produce progeny after coinfect E. coli K (where neither mutant can lyse the host by itself). The rII group of mutants studied by Benzer does not produce plaques on <em>E. coli</em> K strains that carry phage λ (lysogenic for λ), but they produce plaques on <em>E. coli</em> B strains. This study showed that rIIA and rIIB are different genes and/or cistrons in the rII region.
