Micro 8 Flashcards

1
Q

What are the four types of viral RNA structure?

A

+ssRNA, -ssRNA, dsRNA, and circular -ssRNA

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2
Q

What are capsids?

A

proteins shells that hold viral nucleic acid

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3
Q

What are the main types of capsids?

A

helical, icosahedral, and complex

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4
Q

Describe helical capsids.

A

concerted assembly in which proteins of the capsid bind to nucleic acid as the nucleic acid alpha helix is being constructed (all happening at the same time). Proteins don’t spiral because they are bound to the alpha helix structure. Length of the capsid is determined by the length of the nucleic acid helix

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5
Q

Describe icosahedral capsids.

A

These are made in a sequential mechanisms known as headful packaging. Triangle shaped monomer proteins self-assembly to form pentamers and then those will self-assembly to form a pro-capsid, which has gaps for nucleic acid insertion. Following nucleic acid insertion, the mature capsid will form and seal. called headful because the size of the capsid is made to fit one genome inside. If the genome is too large, pressure will build and the capsid will burst

maximizes volume to surface area without internal support needed

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6
Q

What are naked viruses?

A

genome+ capsid= nucleocapsid is the final structure with no envelope. Commonly have spike proteins for attachment and are virulent in that form

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7
Q

What are enveloped viruses?

A

Some viruses have lipid envelopes that are derived from cellular membranes so the nucleocapsid is not the infectious portion. Loss of the lipid envelope causes loss of infectious nature. In the envelope, the protein content (typically glycoproteins) are encoded by the virus themselves and inserted in the envelope. These mediate virus attachment and integration, so the loss of the envelope is bad for the virus.

never stable in GI and require a wet environment for spread

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8
Q

What are the main steps of virus replication?

A

1) attachment and penetration
2) uncoating
3) early transcription and synthesis of nonstructural proteins (for DNA and RNA viruses)
4) genome replication
5) late transcription and synthesis of structural proteins
6) assembly and release

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9
Q

What are the two main ways viruses enter cells?

A

endocytosis (ph-dependent) and plasma membrane fusion (ph-indepedent)

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10
Q

How does viral endocytosis work?

A

Enveloped virus (most naked viruses use this route) attaches to the surface via spike proteins and invaginate into the cell in an endosome. As the endosome matures from an early to a late endosome, the pH lowers, triggering conformational changes in the protein coat of the virus and it fuses with the endosome, releasing the nucleic acid into the cell.

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11
Q

How does plasma membrane fusion work?

A

pH-independent. Almost always used by enveloped viruses. Fusion glycoprotein in the envelope of the virus causes release of nucleic acid into the cell from the cell surface without the use of endosomes

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12
Q

What is early transcription?

A

transcription that occurs before genome replication and the point is to transcribe proteins that produce non-structural proteins (i.e. proteins needed for genome replication)

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13
Q

Where do RNA encoded viruses replicate?

A

the cytoplasms because they don’t need much from the nucleus

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14
Q

Where do DNA encoded viruses replicate?

A

the nucleus (with some exceptions)

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15
Q

What is late transcription?

A

transcription of structural proteins after genome replication

Naked viruses will then lyse the cell to be released. Enveloped viruses will likely bud from the cellular membrane which forms around it (so it derived from the host cell)

Remember: naked viruses will lyse the cell to leave

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16
Q

What is the eclipse period of viruses?

A

only occurs in viruses, not intracellular bacteria. From 2-10 hours at the start of viral infection where a virus cannot be detected inside or outside the cell.

At 2 hours all the virus has entered the cell and uncoated so that intracellularly we can’t detect the viral presence. At 10 hours after genome replication (at about 8 hrs) viruses produce/assemble the intracellular progeny virus and we can detect it.

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17
Q

When can viruses be detected extracellularly?

A

about 16 hrs when the progeny are released (the end of the latent period)

Latent period= time where viruses can’t be detected extracellularly

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18
Q

T or F. RNA viruses must encode their own RNA-dependent RNA polymerase

A

T. Because the template they are providing is RNA and we use a DNA template

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19
Q

Retroviruses must encode what?

A

reverse transcriptase (think HIV)

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20
Q

What is the difference between small and large DNA viruses in terms of DNA polymerase?

A

Small DNA viruses (HPV )do not have their own DNA polymerase because they are too small and can’t encode them so they use proteins that alter our DNA polymerase for their own use, while large DNA viruses (herpes) can encode their own (we can target these)

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21
Q

How does +ssRNA replication occur?

A

A ribosome will enter the genome via a ribosomal entry site at the 5’ end and translate (TRANSLATION FIRST) a protein that is a polyprotein containing capsid and pol. Then cleavage occurs on the polypeptide (sometimes the protease is virally encoded and sometimes from the host cell). The cleaved polymerase molecule will then recognize the viral genome as a template for the production of additional strands of 3’-5’ RNA (complementary to viral genome) and then that strand can be used to make many (+) 5’-3’ RNA progeny strands. Some of those stands will become messenger RNA for continued translation of proteins to make capsid proteins that will come together to form nucleocapsids that may or may not be enveloped

22
Q

How does -ssRNA replication occur?

A

The RNA-dependent RNA polymerase (can’t encode inside the cell) must come in with the virus to allow synthesis *(TRANSCRIPTION)** of a + strand of viral genome which will serve as mRNA, then translation occurs resulting in individual proteins (not a polypeptide). This allows for production of more RNA-dependent RNA polymerase to make more - strand progenies and additional mRNA for more protein production.

Mature progeny needs negative genome, proteins, AND an RNA polymerase

23
Q

How does retrovirus production occur?

A

these are positive sense single stranded RNA viruses that must bring in their own reverse transcriptase. Reverse transcriptase synthesizes a complimentary DNA strand, gets rid of the original strand, and synthesizes a second DNA strand to make double stranded molecules that integrate into our chromosome to be transcribed by our host RNA polymerase

24
Q

How is viral growth measured?

A

Via plaque assays that measure the “hole” in a confluent monolayer of cells that is left after cell lysis. Cell death grows circularly and can be measured this way

measured as plaque-forming units (pfu)/ml of lysate= titer

This is a biological assay of infectivity. Only get a plaque if the viral particle is infectious. Not all viruses are infectious.

25
Q

What is lysate?

A

a suspension of visions in culture medium that results from unrestricted growth of the virus on a cell monolayer. As more plaques form, they will grow together and we can a suspension of the virus

26
Q

What is Particle-to-PFU ratio?

A

number of particles released to the number of those that a re plaque forming. Animal cells have ratios of 10:1

27
Q

T or F. Viral mutations occur at a relatively high frequency.

A

T. because there are a large number of genome copies and also because of high error rate among RNA polymerase without proof reading ability

28
Q

What is Complementation?

A

can occur in an RNA or DNA virus. Sharing of proteins among infecting viruses that can allow a viral particle with defective proteins to be integrated by using a protein on another virus simultaneously infecting the host cell. Doesn’t genetically fix the defective protein like recombination does.

29
Q

What is Recombination?

A

Exchange of DNA material among viruses that are co-infecting a cell which could result in repair of defective proteins on one or both of the viruses. DNA viruses only (although RNA viruses can do ‘strand transfer” which is similar)

30
Q

What is Reassortment?

A

Limited to RNA segmented viruses. Co-infection of segments of these viruses can result in recombination. Major role in flu virology.

31
Q

What is the most frequent route of infection for viruses?

A

respiratory. Dissemination is via blood, lymph, CSF, and neurons

32
Q

How does localized cell-to cell spread occur uniquely?

A

Can occur uniquely: When enveloped viruses bud through a membrane they acquire glycoproteins. Herpes viruses and others (respiratory sensitial) can put a fusionogenic proteins that functions in a pH-independent manner on the host cell membrane that allows them to fuse to adjacent cells (called sensitia formation- HIV can do this too). Direct fusion without release of virus and re-infection of another cell

think gp120 binding to CD4 on HIV

33
Q

T or F. Most viral infections completely resolve without virus-specific treatment.

A

T. Persistent infections are key for some diseases, especially in immune deficiency

34
Q

What are some types of persistent viral infections?

A

1) Chronic (productive), eg hep B or C- equilibrium reached with our immune system and not leading to significant stress in a person
2) Latent, eg herpes- certain time when the virus cannot be detected because it is not reproducing but is always present in host cell genomes and can come back under stress
3) Transforming, eg papiloma- cancer causing

35
Q

Immune response of viruses

A

Many of the symptoms seen from viruses are the result of our own bodies attempt to resolve the infection. Our body uses the IFN-alpha pathway

36
Q

Describe the IFN pathway

A

A cell has bound IFN from a virally infected cell. When binding occurs, the IFN pathway is induced. Study pathway.

The pKR and 2-5A synthatase pathways are only FULLY activated by viral double-stranded RNA in that cell. Keeps the cell from killing itself when not infected

PKR pathway shuts down ALL protein synthesis (host and viral) and 2-5A syntheses cleaves ALL RNA in the cell, so a fully activated IFN pathway response will kill the cell to limit the infection

These pathways help limit the spread of the viral infection

37
Q

Vaccines

A

Not practical if a large number of strains cause a disease or if a virus exhibits variation in a dominant antigenic structure (e.g. hep C where a 30 AA stretch can mutate to avoid our antibody response so we have to constantly adapt to control it)

38
Q

What are the types of vaccines?

A

killed, live attenuated, and other subunits

39
Q

Advantages of live vaccines?

A

can give orally (vs. injecting in killed), dose can be lower, often only one dosing needed (killed need boosters), immunity lasts longer, can get a IgA response (killed only get an IgG response so they don’t inhibit the SPREAD of disease if you poop out the bug)

40
Q

Disadvantages of live vaccines?

A

heat labile, can become virulent on occasion and cause disease

41
Q

Subunit vaccines?

A

viral proteins purified for use in papiloma (HPV) and hepatitis (HBV) vaccination. cannot cause disease, not derived from blood, but do require multiple injections to boost immune response

42
Q

What are some live vaccines?

A

Polio (oral), measles, mumps, rubella, varicella-zoster (chickenpox-shingles), influenza (inhaled), small pox

43
Q

What are some killed vaccines?

A

Polio (injected), influenza (injected), Hep A, rabies

44
Q

What are some subunit (yeast-derived) vaccines?

A

Hep B and HPV (can be considered anticancer vaccines)

45
Q

What is the basis of passive vaccination?

A

Can give immune globulin to protect people immediately so immune response does have to be formed in case of pre- and post- exposure prophylaxis

Post-exposure uses include: Hep A or B, measles, rabies, chickenpox

46
Q

What are some of the consequences of enveloped viruses vs. non-enveloped ones?

A

Envelops are made of lipids that are less stable than the capsids of non-enveloped viruses so they are more sensitive to detergents, heat, and the acidity of the GI tract (so if you see GI distress caused by virus, you know its not an enveloped virus)

Spread through droplets, secretions, blood transfusions, lymph

They do help disguise the virus from the host because the sugars on the glycoproteins are from the host.

47
Q

What are prions?

A

infectious proteins

48
Q

Why do viruses use repeating subunits (capsomeres) to build their capsids?

A

This allows them to maintain a small genome

49
Q

What must almost every RNA virus encode to replicate its genome?

A

RNA-dependent RNA polymerase

retroviruses need reverse transcriptase

50
Q

Why can we target nucleoside inhibitors for herpes and not for HPV?

A

Herpes virus is large enough to encode its own DNA polymerase while HPV is too small and has to use/alters ours so it’d be toxic to target it

51
Q

T or F. DNA viruses use host RNA polymerase II transcribing viral genes.

A

T. They modify it for preferential use