21.1 Viral Evolution, Morphology, and Classification

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Last updated 12:41 PM on 8/25/26
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26 Terms

1
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What did Ivanowski's 1892 experiment prove?

The Chamberland-Pasteur filter removed every visible bacterium, but the extract still gave healthy tobacco plants the disease. So the agent had to be something smaller than bacteria.

2
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Why weren't viruses seen until the late 1930s?

Virions run 20–250 nm, too small for light microscopes. The electron microscope gave the first real look, starting with TMV.

3
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Scanning vs. transmission EM?

Scanning shows surface structure only. Transmission is the only way to see what's inside a virion.

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Why is virus origin harder to study than most evolutionary questions?

Viruses don't fossilize, so there's no historical record. Scientists have to work backward from how modern viruses evolve.

5
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Regressive ("devolution") hypothesis?

Viruses started as free-living cells or intracellular parasites and lost complexity over time. Basically: they shrank down into viruses.

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Progressive ("escapist") hypothesis?

RNA/DNA molecules or mobile elements like transposons escaped from a host cell and gained the ability to enter another one.

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Virus-first hypothesis?

Viruses were the original self-replicating entities, existing before the first cells did.

8
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Why do most scientists reject a single common ancestor for viruses?

There's no genomic sequence that all viruses share. That points to multiple separate origins rather than one lineage.

9
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Capsid vs. capsomere?

The capsid is the entire protein coat around the genome. Capsomeres are the individual protein subunits that build it, and they're encoded by the viral genome itself.

10
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Where does a viral envelope come from?

It's protein and phospholipid membrane taken from the host cell — the virus doesn't manufacture it.

11
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Does a more complex host mean a more complex virus?

No, there's no correlation. Bacteriophages infect the simplest organisms and include some of the most elaborate virions known, like T4.

12
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Why are non-enveloped viruses harder to destroy?

Envelopes are fragile, so enveloped viruses break down more easily under heat, pH changes, and some disinfectants. Non-enveloped ones like polio and hep A survive rougher conditions.

13
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What can't you conclude from a virus's shape and envelope status?

What disease it causes or what species it infects. Morphology is a classification starting point, not a predictor.

14
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Why is "viral receptor" a slightly misleading name?

These are ordinary host molecules with their own normal functions. Viruses simply evolved to exploit them — cells didn't evolve receptors for viruses.

15
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What does CD4 actually do, and how does HIV use it?

CD4 is a cell adhesion molecule that keeps immune cells near each other during a T lymphocyte response. HIV binds it to get into T cells.

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How do adenovirus and influenza attach differently?

Adenovirus is non-enveloped and uses glycoprotein spikes sticking out from its capsomeres. Influenza is enveloped and uses glycoproteins embedded in the envelope.

17
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What do influenza's matrix proteins do?

They sit just inside the envelope and stabilize the virion's shape. They also help assemble new virions.

18
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Why do RNA viruses mutate faster than DNA viruses?

RNA polymerases make copying errors more often than DNA polymerases do. That means faster mutation and faster adaptation to the host.

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Why is influenza so hard to vaccinate against?

Its RNA genome is segmented rather than one continuous piece, which drives constant variability and ongoing evolution.

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Why are viral genomes so small?

They only encode proteins the virus can't get from the host cell. Everything else is borrowed from host machinery.

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What do RNA viruses have to supply that DNA viruses don't?

Their own replication enzymes — RNA-dependent RNA polymerase, or reverse transcriptase in retroviruses. DNA viruses just direct the host's existing replication proteins.

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Why can't 16S rRNA be used to classify viruses?

It's a ribosomal sequence, and viruses have no ribosomes. More broadly, viruses share no universal sequence to compare.

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What is Baltimore classification based on?

How each virus produces mRNA during its replication cycle, rather than shape or genome type.

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Why is that a better basis than morphology or nucleic acid type?

Every virus has to make mRNA, so it's the one step they all share. The older systems keyed on different features and produced conflicting groupings.

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Positive vs. negative polarity in ssRNA viruses?

Positive (Group IV) means the genome reads like mRNA and can be used directly. Negative (Group V) means it's complementary, so it must be transcribed before translation.

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Groups VI and VII both use reverse transcriptase — what's the difference?

Group VI (HIV) starts as ssRNA, reverse transcribes into dsDNA, and integrates into the host genome. Group VII (hep B) starts as partial dsDNA and replicates through an RNA intermediate.