Importance of Viruses
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Importance of Viruses







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Cause many diseases in plants, animals & humans Some viruses are easily controlled with a vaccine Mumps, Measles, Smallpox, Polio Some viruses are difficult to control with a vaccine Retroviruses (HIV: ssRNA  dsDNA) Common cold, Influenza (Flu), HIV Used as vectors in biotechnology
Importance of Viruses

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Slide 1

Cause many diseases in plants, animals & humans

Some viruses are easily controlled with a vaccine

Mumps, Measles, Smallpox, Polio

Some viruses are difficult to control with a vaccine

Retroviruses (HIV: ssRNA  dsDNA)

Common cold, Influenza (Flu), HIV

Used as vectors in biotechnology

Used to insert therapeutic genes into a host cell chromosome

Use viruses with provirus in life cycle

Importance of Viruses

Slide 2

Herpes(dsDNA  dsDNA)

Cold sores

Herpes virus may rest inactive inside host cells for long periods

Slide 3

Adenovirus (dsDNA)

Adenoviruses cause various respiratory diseases

Slide 4

Polio Virus(ssRNA serves as mRNA)

Polio is easily prevented with a vaccine

Slide 5

Measles(ssRNA template for mRNA synthesis)

Measles: a childhood disease that can be prevented with a vaccine

Slide 6

Couple at AIDS quilt (HIV: ssRNA  dsDNA)

HIV is very difficult to control with a vaccine

Slide 7

1918 Influenza epidemic(ssRNA template for mRNA synthesis)

>20 million died of the flu during WW I

A new influenza vaccine must be developed yearly

Slide 8

Influenza Today

Slide 9

Enter H5N1, the avian flu virus

Slide 15

Why do new strains of influenza and bird flu arise in Asia?

Slide 16

Background: Influenza Virus Structure (1 of 3)

  • Flu viruses are named by the type of surface proteins

    • Hemagglutinin

      • Helps virus enter cell

      • Type A infects humans, birds and pigs

      • Type A has ~ 20 different sub types

  • Flu Viruses Currently infecting...

  • Humans: H1N1, H1N2, and H3N2

  • Avian Flu Virus: H5N1

Slide 17

Background: Influenza Virus Structure (2 of 3)

  • Named for the type of surface proteins

    • Neuraminidase

      • Helps virus exit cell

      • 9 subtypes

  • Currently infecting Humans:

  • H1N1, H1N2, and H3N2

Slide 18

Background: Influenza Virus Structure (3 of 3)

  • Influenza viral genome

    • ssRNA

    • 8 segments (pieces)

    • One gene per segment

  • Avian Flu Virus: H5N1

    • Transmitted from birds to humans

    • No evidence of human to human transmission

    • Antiviral drugs: Tamiflu

      • a neuraminidase inhibitor

      • Consequences of its action?

Slide 19

Antigenic drift – due to errors in replication and lack of repair mechanism to correct errors

Results in ___________________ changes

Antigenic shift - reassortment of genetic materials when concurrent infection of different viral strains occurs

Results in ___________________ changes

Genetic Changes in Influenza Viruses

Slide 20

Emergence of New Influenza Subtypes: H5N1

Antigenic shiftdue to genome reassortment within intermediate hosts drives flu epidemics and pandemics

Solid lines: transmission demonstrated;

Dotted lines: transmission postulated but not demonstrated.

Source: http://www.cdc.gov/ncidod/EID/vol12no01/05-1024-G1.htm

  • Nonpathogenic H5 influenza virus: Wild fowl  domestic ducks and geese,  domestic chickens.

  • H5 virus became highly pathogenic in chickens  domestic ducks and geese.

  • Highly Pathogenic H5 virus reassorted its genome with those of other influenza viruses in aquatic birds,  spread to poultry farms, humans, and occasionally to pigs.

Slide 21

Where do the “new flu” viruses come from?

Antigenic Drift:mutations result in changes to the Hemagglutinin (HA) molecules

  • - RNA replication is error prone

  • - New HA types are created frequently

  • Requires new vaccine every “season”

  • What is a vaccine?

Slide 22

What is a vaccine?

Vaccines stimulate the production of memory cells

Give long-term protection against a specific antigen

Why are vaccines ineffective against the flu virus?

Why will this year’s flu vaccine be ineffective next year?

Why are vaccines effective against DNA viruses?

e.g. small pox and polio virus

Vaccines: Protection against viruses

Slide 23

Smallpox (dsDNA  dsDNA)

Smallpox has been irradicated worldwide due to a very successful vaccine

Why are vaccines for DNA viruses so successful?

Slide 24

Hepatitis B—an RNA virus

Hepatitis B

Infections may lead to liver cancer. Why?

Carry viral oncogene

Slide 25

Tumor Viruses: may transform normal cells into cancer cells

Hepatitis B Liver cancer

HTLV 1 leukemia (Human T-Cell Leukemia Virus)

Tumor viruses form a permanent provirus

Viral oncogenes

code for growth factors

Growth factors Stimulate cell to enter S phase

G1 or G0 S phase

Each of the following must happen for cancer to occur

Active host oncogenes + Active viral oncogenes  cancer

Activators of host oncogenes

Carcinogens, radiation, some viruses

Viruses and Cancer

Slide 26

Emerging viruses

Ebola Virus

Hanta Virus

Both viruses: ssRNA template for mRNA synthesis

Either virus usually results in death within days!

Slide 27

Deer Mouse: Carries Hanta virus in Feces

Slide 28

Mottling of Squash and Tobacco by the Mosaic Virus

Viruses can spread easily from cell to cell via the plasmodesmata junctions between cells

Slide 29

Tobacco mosaic virus (RNA virus)

Slide 30

Comparing the size of a virus, a bacterium, and a eukaryotic cell

  • Viral Size

  • Millions can fit on pinhead

  • Smaller than a ribosome!

Slide 31

Viral structure

TMV Adenovirus Influenza virus Bacteriophage T4

Slide 32

Nucleic Acid + Protein Coat (Capsid)

Some viruses with Membrane (envelope) surrounding capsid

Envelope derived from plasma membrane of host cell

Helps virus infect host cell

No organelles

Obligate intracellular parasite

Lacks metabolic enzymes, ribosomes, mitochondria

Alone, can only infect host cell

Nucleic Acid: DNA or RNA

Single or Double Stranded

4 genes to a few hundred

Viral Structure

Slide 33

Classes of Animal VirusesGrouped by Type of Nucleic Acid

Slide 34

Host cell Recognition

Complementary fit between external viral proteins and host cell surface proteins

Some have a Broad host range

Swine flu and rabies viruses

Some have a narrow host range

Single tissue in a single species

e.g. Adenovirus, HIV

Phages of E. coli

Host Range

Slide 35

Simplified DNA Virus Life Cycle

E.g. smallpox, herpes, chickenpox

“Lock and Key” fit between viral surface proteins and host cell receptors initiates endocytosis

Viral Reproduction

Slide 36

Electron micrograph of Bacteriophage T4

Bacteriophages are viruses that infects bacteria

Slide 37

Bacteriophages (Bacterial Viruses)

Best understood of all viruses

Responsible for many advances in molecular biology

Hershey-Chase expmts that showed that DNA is the genetic material

Restriction Enzymes used in Genetic Engineering come from bacteria

Lytic Cycle of Bacteriophage T4

T4 is a Virulent Phage

Lyses host  death of host cell

Bacteriophage Reproduction

Slide 38

The lytic cycle of phage T4

Slide 39

Lytic and Lysogenic reproductive cycles of phage , a temperate phage

What is the adaptive value of forming a prophage?

Lysogenic

Cycle

Lytic

Cycle

Prophage

Slide 40

RNA viruses

RNA serves as template to produce mRNA

e.g. viruses that cause rabies, measles, mumps, flu

DNA viruses

DNA serves as template to produce mRNA

Herpes (Cold sores, genital herpes)

Smallpox

Adenovirus

The reproductive cycle of an enveloped Virus

Slide 41

AIDS: Acquired Immunodeficiency Syndrome

  • AIDS—caused by HIV infection

  • HIV = Human Immunodeficiency Virus

HIV infecting a Helper T-Cell

Slide 42

HIV infection

Slide 43

AIDS around the world (Source: UNAIDS)

Slide 44

The Structure of HIV: A Retrovirus (RNA virus)

Envelope protein

Carbohydrate

Lipid envelope

Reverse

Transcriptase

Protein

Capsid made of protein

RNA

(2 copies of its genome)

Slide 45

Animation of HIV Life Cycle

Questions to Address:

  • Why does HIV infect a specific cell type,

    T-helper cells (CD-4 cells)?

  • What is HIV’s Genetic material?

  • What are the roles of Reverse Transcriptase, integrase, and protease?

  • How can knowledge of HIV’s life cycle be used to develop anti-HIV treatments?

  • Reverse Transcriptase does not “proof read” like DNA polymerase does.

    • What are the consequences?

    • Of what adaptive value is this?

Slide 46

HIV primarily infects T-Helper Cells!

  • Why does HIV have a narrow host range?

  • Why does the virus that causes rabies have a broad host range?

3.) Infection

HIV

2.) Fusion

1.) Binding

Envelope

protein

Capsid

RNA

CD4

Receptor

protein

Cytoplasm of white blood cell

(T-Helper Cell)

Helper protein

Plasma membrane of T-helper cell

Slide 47

What’s happening?

1.

2.

3.

4.

5.

6.

Reverse transcriptase

Overview of HIV’s Reproductive Cycle

DNA of host cell

Viral RNA

Provirus DNA

1

DNA strand

Nucleus

2

Double-stranded DNA

3

4

5

Viral RNA and proteins

Cytoplasm

6

Slide 48

Reproductive Cycle of HIV—the details!

HIV

Entry

Reverse transcriptase

Viral RNA

Viral RNA

copied

to viral DNA

Integrase

Viral DNA

integrates into

cell chromosomes

andmakes more

viral RNA

Viral RNA

Synthesis

of HIV proteins

Protease cleaves large

proteins into smaller ones

HIV envelope proteins

come to cell surface

HIV assembles

and buds from cell

Slide 49

Treatments for HIV

  • Vaccines have beenunsuccessful—why?

  • Reverse Transcriptase Inhibitors Block viral DNA formation from viral RNA

  • DNA base analogs Block DNA elongation

    • e.g. AZT, 3TC (3-thiocytosine)

  • Protease Inhibitors Block enzymes that process envelope proteins

  • Why use a “Shotgun” approach?

  • Possible future treatments:

    • Plug drugs—drugs that plug receptors for HIV on surface of host cell

    • Vaccines

Slide 50

Evolved from fragments of Cellular Nucleic Acids

Evidence

Viral genetic material similar to host cells genetic material

Some viral genes are identical to host’s genes

Eukaryotic viral genetic material is quite different to prokaryotic and phage genetic material

Eukaryotic viral genetic material is similar to transposons (“jumping genes”)

Transposons: highly mobile eukaryotic genetic material

Phage DNA is similar to Plasmid DNA

Plasmid DNA: highly “mobile” extra-chromosomal circular DNA found in bacteria

Evolutionary Origin of Viruses

Slide 51

Lysogenic Conversion

Expression of prophage genes to produce toxins

Botulism

Bacterium  neurotoxin (coded by prophage)  paralysis  death

Are antibiotics effective against botulism poisoning?

Scarlet Fever

Bacterium  toxin (coded by prophage)  sore throat, strawberry-colored tongue, rash  death

Give antibiotics within 3 days

Lysogenic Conversion


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