Virions, Prions, and Viroids: Infectious Agents of Animals and Plants Topics Structure...

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Virions, Prions, and Viroids: Infectious Agents of Animals

and PlantsTopics

Structure

Classification

Methods of study

Viral infections

Viral tumors

Human tumors

Viral host range

Prions

StructureAnalogous to bacteriophages• Capsid (protein coat) made up of capsomeres• Naked vs. enveloped viruses• Attachment proteins or spikes in enveloped viruses

Distinct from bacteriophages• Segmented viruses (contain more than one RNA

molecule)• Plant viruses do not enter via receptor attachment

Shapes:IsometricHelicalPleomorphic

Classification

Taxonomy in constant fluxMost common taxonomic criteria for animal viruses:

1. Genome structure (DNA or RNA, ss vs. ds, segmented or not)

2. Virus particle structure (isometric, helical, pleomorphic)

3. Presence or absence of viral envelope

Viruses infecting vertebrates are divided into 14 RNA families and 7 DNA families (Ending: -viridae)

Coronavirus

• Classification: – Coronaviridae (Family) – Coronavirus (Genus)– Common cold virus (Species) (together

with rhinoviruses)

• Structure: – non-seg., lin., ssRNA, helical, env.

Cells Infected with a Herpes Virus

Groupings Based on Routes of Transmission

Not a taxonomic grouping – more than one family may be included in one transmission grouping

Methods of Study

Much more expensive and difficult to study animal viruses than bacteriophages

• Cultivation in host cells– Living animal– Embryonated chicken eggs– Cell or tissue culture (= in

vitro)

Methods of Study cont: Quantitation• Plaque assay (useful for infective and lytic viruses)

• Virion counting with EM

• Quantal assay (ID50 or LD50)

• Hemagglutination (e.g.influenza virus)

Acute Viral Infections

Productive infection of relative short duration

Naked viruses usually cause cell lysis, while enveloped viruses do not

Symptoms due to localized or widespread tissue damage

Host defense mechanisms gradually eliminate virus

Examples of acute infections

Time course

Mumps, Measles, Influenza, and Poliomyelitis

Time Course of Acute Viral Infection

HEV

Reproductive Cycle

1. Attachment

2. Entry

3. Uncoating

4. Replication of NA and protein

5. Maturation of viral particles

6. Cell lysis

7. Spreading and shedding

8. Transmission to next host

Transcription Strategy

Mechanisms of Release

1. Cytopathic effect: Unlike virulent phages most animal viruses do not encode for cell lytic enzymes. Instead degenerative changes associated with the virus lead to cell death.

2. Budding: from plasma membrane (most common) or from Golgi apparatus. May or may not kill cell. Enveloped viruses

Persistent Viral Infections

Virus continually present in body. Released by budding.

May or may not cause disease

Carrier able to spread disease

Four categories (if more than one applies = complex infections):

1. Late complications from acute infections2. Latent infections3. Chronic infections4. Slow infections

Late Complications from Acute Infections

1. Subactue sclerosing panencephalitis (SSPE) - years following measles in 1 in 300,000. Virus persistent in brain tissue with decreased transcription of viral genome. Lack of envelope protein production prevents immune response to eliminate infected cells. High Ab, low CMI. Exact mechanism unknown.

2. Progressive (pan)encephalitis following rubella

Latent Infections

• Acute infection symptomless period reactivation of disease

• Symptoms of reactivation may differ from original disease

• No measurable viral particles during symptomless period

• Examples: HSV-1 and HSV-2; varicella

Chickenpox- Varicella

Blister-like rash on surface of skin and mucous membranes. Blisters usually appear first on trunk and face, then spread to almost everywhere else.

Shingles or Herpes Zoster

About 20 % of those people who have had chicken pox will get zoster at some time during their lives. Most people will get zoster only once.

“Shingles” comes from latin cingulum, which means girdle or belt.

It occurs in an area of the skin that is supplied by the sensory fibers of a single nerve- dermatome. Rash appears as well-defined band on one side of body, or on one side of face, arms or legs.

Chronic Infections

• Virus can be demonstrated at all times

• Disease may or may not be present for extended time periods or show up late (carriers!)

Slow Infections

• Gradual increase of infectious agent over long time period – often no apparent symptoms for long time (=preclinical phase)

• Usually slowly progressive lethal diseases

• Examples– AIDS– Lentivirus– prions

HIV: Example of Complex Infection

• Retrovirus – ssRNA, envelope

• RNA DNA (with the help of reverse transcriptase) permanent integration into host genome (=provirus)

• Polyprotein is cleaved into individual proteins with viral protease assembly of virions budding

Viral Tumors (Neoplasms)• Benign

• Malignant cancer, metastasizes

• Proto-oncogenes and oncogenes are regulatory genes

• Properties of normal and transformed cells

• Only about 15% of human tumors are due to viruses

• Examples of human tumors: – Kaposi’s sarcoma (herpes virus)– Squamous cell carcinomas (HPV)– Hepatocellular carcinoma (HBV and HCV)

Kaposi’s Sarcoma

Purplish lesions of a skin cancer not usually seen in young men

Viral Host Range

• Mostly species – and even cell type – specific

• Exception: Zoonotic viruses are transmissible from animals (arthropods, vertebrates) to man (zoonosis) – Arboviruses (West Nile virus), rabies etc.

• Modification of host range due to – Phenotypic mixing– Genetic reassortment

Genetic Reassortent

• In segmented viruses

• Simultaneous infection of one cell with 2 different types of viruses leads to exchange of genetic information

• Creation of major new influenza strains resulting in pandemics

• Antigenic shift vs. antigenic drift

Other Infectious Agents: Prions• Small proteinaceous infectious particles (resist

inactivation by procedures that modify nucleic acids)

• Prion diseases are often called spongiform encephalopathies because of the post mortem appearance of the brain with large vacuoles in the cortex and cerebellum

• Human prion diseases– CJD: Creutzfeld-Jacob Disease– BSE: Mad cow disease (BSE)– GSS: Gerstmann-Straussler-Scheinker syndrome – Kuru

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