BIO3710 Chapter 6 Viruses

virus

acellular, infectious agents that require a host to replicate

what are the main components in a virus

DNA and RNA in a protein coat called a nucleocapsid

capsid composed for protomers

nucleic acid codes for viral protomers

bacteriophage

a type of virus that uses bacteria as its host

virion

a complete virus particle containing a protein capsid surrounding one nucleic acid molecule

cannot reproduce independent of living cells nor carry out cell division

they can exist extracellularly

virus morphology

capsid symmetry and presences of envelope

helical capsid

icosahedral capsid

complex symmetry

viruses without a helical or icosahedral capsid (pox virus and large bacteriophages)

envelope

outer membranous layer made of lipids from host and proteins coded from viral genes that project (peplomers or spikes)

pleomorphic

the envelope can have ability to be very fluid

influenza’s two spikes and function

hemagglutinin: attach to host cell

neuraminidase: release mature virus from cell

envelop or capsid enzyme function

involved in nucleic acid replication

types of viral genomes

DNA (linear or circular)

• ssDNA (rare)

• dsDNA- most bacteriophages and archaeal viruses, many animal viruses

RNA

• ssRNA: (+) and (-) sense and retroviruses

• dsRNA (fewer)

steps to viral multiplication

1. attachment to host cell

2. entry and uncoating of genome

3. synthesis

4. assembly

5. release

1. Attachment

specific receptor attachment determined by preferences of specific tissue, number of hosts, and number of receptors

2. entry

envelope will either fuse with the plasma membrane or through endocytosis

3. synthesis and 4. assembly

virus goal is to replicate genome and translate it to protein

genome dictates where is needs to go

• DNA virus: nucleus

• RNA virus: cytoplasm

• Retrovirus: nucleus

5. Release

depends on presence of envelope

non-enveloped: lyse the host cell

enveloped: bidding

neoplasia

abnormal cell growth due to loss of regulation

tumor cells

excessive proliferation and loss of differentiation (anaplasia)

carcinogenesis

oncogenes: leads to cell division of cancer cells

proto-oncogenes: normal growth genes that become oncogenes

oncovirus

viruses that trigger cancer in host

ex. HPV → cervical cancer

4 types of animal viruses infections

Acute

Persistent (latent and chronic)

transformation into malignant cells

Acute infection

access to cell → rapid multiplication → cell death and release (cytocidal)

symptoms are from immune system fighting infection (congestion, exhaustion, vomiting)

resolves quickly compared to other forms

ex. common cold

Persistent latent infection

virus gets in → deactivates → reactivates into acute

ex. herpes

persistent chronic infection

virus gets in→ slow replication→ release without cell death

very slow infection

ex. hepatitis C and HIV (can become latent)

Transformation into malignant cell

latent or chronic → cancerous cell

cytopathic effects- cause microscopic or macroscopic degenerative changes or abnormalities in the cell

oncovirus mechanism

tumor suppressor proteins

• regulate cell cycle and repair DNA damage

viral protein inactive tumor suppressor proteins

• Rb: nuclear cell cycle protein

• p53: responds to DNA damage

viruses carry oncogenes

integrate near proto-oncogenes→ proliferation

virulent phage

one reproductive choice

multiplies immediately upon entry

lyses bacterial host cell

temperate phage

have two reproductive options

reproduce lytically as virulent phages do

remain within host cell without destroying it

• many integrate genome into host genome (becoming s prophage in a lysogenic bacterium)

• lysogeny

lytic cycle

Remember: NONSTOP

lysogenic cycle

remember: WAIT FOR IT

Lysogenic Conversion

temperate phage change phenotype of host

• bacteria becomes immune to superinfection

• phage may express pathogenic toxin or enzyme

under appropriate conditions infected bacteria will lyse and release phage particles → induction

• changes in growth conditions and UV irradiation

2 advantages to lysogeny

1. can protect themselves by leaving cell

2. bacteria becomes immune

characteristics of archaeal virus

can be virulent or temperate

chronic infections

little known about replication cycle

A newly isolated virus has been analyzed for its chemical structure, and has been found to contain DNA, protein, and lipids. Based on this information, identity its type by choosing the best answer below.

A. Enveloped virus

B. naked icosahedral virus

C. naked virus

D. enveloped icosahedral virus

A. enveloped virus has lipids

B. naked icosahedral cannot have lipids

C. naked virus cannot have lipids

D. enveloped icosahedral virus nothing can prove shape in what is given

A bacteriophage population is introduced to a bacterial colony that is in stationary phase with rapidly depleting nutrients. Appraise the following scenarios and select which one would favor long-term survival of the bacteriophage.

A. the bacteriophages do not infect the bacterial cells since they are dying; they remain inert outside of the cells.

B. the bacteriophages infect and lyse the viable bacterial cells to increase their number while they have an available host

C. the bacteriophages infect the remaining viable cells and integrate their genetic material into the host cell genome, thereby preserving their genome

A: does not favor long term survival because they die due to nutrient depletion and would have not time to replicate their genome leading to the inert stages death over time

B: would only lead to short term phage growth and accelerated host cell death which would lead to no hosts and eventually dying out

C: allows bacteriophage to preserve genome in the bacterial cell. though the colony will deplete there will still be dormant cells in the host cell, therefore preserving the survival of the bacteriophage

which of the following statement regarding a latent viral infection are TRUE? Select all that apply.

A. During a latent viral infection, viruses are rapidly multiplying

B. Viral DNA is present during a latent viral infection

C. During a latent viral infection, viruses are being released slowly, but the host cell does not die

D. viral oncogenes are always expressed during a latent viral infection

E. latent viruses can be activated, resulting in an acute viral infection

A. During a latent viral infection, viruses are rapidly multiplying this is an acute infection

B. Viral DNA is present during a latent viral infection

C. During a latent viral infection, viruses are being released slowly, but the host cell does not die this is a chronic infection

D. viral oncogenes are always expressed during a latent viral infection NOT ALWAYS

E. latent viruses can be activated, resulting in an acute viral infection

which of the following is not a mechanism by which viruses cause cancer?

A. they carry a cancer-causing gene into the cell

B. they encode protein that bind to and inactivate host tumor suppressor proteins

C. They produce defective particles

D. They express viral proteins that result in an abnormal expression of genes that regulate cell growth and reproduction

A. they carry a cancer-causing gene into the cell this is a mechanism used by retroviruses

B. they encode protein that bind to and inactivate host tumor suppressor proteins this mechanism is used by many viruses like HPV

C. They produce defective particles do not directly cause oncogenes

D. They express viral proteins that result in an abnormal expression of genes that regulate cell growth and reproduction viruses can do this to activate host oncogenes

Bacteria Cultivation

1. mix cells and virus

2. plate on appropriate media

3. infected cells lyse, releasing virus

4. infect nearby cells, clearing agar

Animal Bacteria

grown in culture with animal cells

plaques formed when cells lyse

• stain with dyes to distinguished living from dead

cytopathic effects detected

Direct Method of Enumeration

electron microscope

quantitative PCR (qPCR)- amplify viral nucleic acid

Indirect Method of Enumeration

Plaque Assay

• similar to spread/pour plate for bacterial titer

• ONLY for quantitate infectious virus particle

Baltimore Viral Class I

dsDNA- HPV and Herpes

Baltimore Viral class II

ssDNA → dsDNA- Parvovirus

Baltimore Viral Class III

dsRNA- rotavirus

Baltimore Viral Class IV

(+)-sense RNA → (-)-sense RNA SARS-Cov-2, polio

Baltimore Viral Class V

(-)-sense RNA- influenza

Baltimore Viral Class VI

ssRNA→ retrovirus→ DNA/RNA→ dsRNA HIV

Baltimore Viral Class VII

dsDNA→ retrovirus- Hepatitis B

Antigenic drift

minor antigenic changes with epidemic potential

Antigenic shift

2 viruses infecting the same cell causing reassortment

major antigenic change via direct jump, adaptation, and genetic assortment

ex. influenza and COVID-19

Virus-First Hypothesis

viruses predate cellular life and represent ancient self-replicating molecules that co-evolved with early cells

• RNA viruses and RNA world

Pro and Con Virus-First Hypothesis

PRO: explains why all domains of life have viruses

CON: viruses need hosts to replicate, so how could they exist before cells

Regressive (Reduction) Hypothesis

viruses started as more complex, free-living organisms that lost genes over time

• giant viruses like Mimivirus have metabolic genes

Pro and Con of Regressive (reduction) Hypothesis

Pro: explains complex viruses with large genomes

Con: does not explain small, simple RNA viruses

Progressive (escape) Hypothesis

viruses originated from genetic elements (like plasmids or transposons) that “escaped” cells and gained ability to move between hosts

• retrotransposons resemble retroviruses

Pro and Con of Progressive (Escape) Hypothesis

Pro: explains how simple RNA viruses and retroviruses could have arisen

Con: harder to explain very large viruses

Virulence-Transmission trade off

virulence must be balanced by transmission