Micro Unit 4B: Viruses

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PROPERTIES OF VIRUSES

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1) Obligate intracellular parasites of bacteria, protozoa, fungi, algae, plants, animals. (ie. must enter a host to reproduce).
2) Ultramicroscopic size, 20-450nm. (smallest bacteria is 400nm). Electron microscope required to examine them.
3) Not cellular in nature. Are acellular.
4) Don't independently fulfill characteristics of life
5) Inactive (dormant) outside host cell, active inside
6) Structure is a protein shell (capsid) surrounding nucleic acid core.
7) Nucleic acid is DNA or RNA, double stranded or single stranded.
8) Molecules on virus surface impart high specificity for attachment to host cell. (infect a certain sp.)
-cross sp transmission in some circumstances
-cross kingdom not known to occur
9) Multiply by taking control of host cell's genetic material and regulating synthesis of new viruses.
10) Lack enzymes for most metabolic processes.
11) Lack machinery for synthesizing prteins.

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3. Outline the classification of human viruses

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Classified ased on viral genome content: RNA and DNA viruses.
1) RNA Viruses
-common resp viruses: influenza, SARS, rhinovirus
-common gi viruses: norovirus, rotavirus
-common other viruses: Hep A, HIV, myocarditis
2) DNA Viruses
-common sti viruses: Herpes, Hep B, HPV
-common resp virus: adenovirus
-common other virus: smallpox

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EFFECTS OF VIRUS INFECTION ON HOST CELL

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1) Inapparent effect - virus lives dormantly in host
2)Cytopathic effect (CPE) - pathological changes to cells causing cell death
a) inclusion bodes - abnormal structure sim to a vacuole in cell cytoplasm filled with new virus
eg. negri bodies occur in nerve cells from rabies
b) Giant cell/Syncytium - infected cells fuse with other cells to spread virus, producing multinucleated giant cells
eg. respiratory synctial virus - common cause of bronchitis, pneumonis
3) Hyperplastic effect - cell stimulated to divide prior to death
4) Transformation - cell stimulated to divide, take on abnormal growth patterns and become cancerous: (altered growth properties): cells growing in multiple layers, loss of contact inhibition, immortalized (continue to multiply indefinitely - do not die after x generations), many form tumors in animals
5) Cell lysis - in vivo cell lysis and death can be cause by virus
-inflammation/immune response
-can lead to loss of normal cellular, tissue, organ fcns, resulting in life threatening conditions
eg. destruction of T/cd4 lymphocytes by HIV is underlying cause of AIDS, increases risk to opportunistic infections and certain cancers (Kaposi's Sarcoma)
-HIV + CD4 cell # <200/uL blood = AIDS (normal level is >500)

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5. Differentiate acute, persistent chronic and latent viral infections and provide examples for each

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1) Acute infection - rapid onset of over S+S, local/systemic, usually shorter duration, recovery due to immunity (virus eradicated from body)
eg. acute hepatitis from HAV
2) Persistent infection - virus always present, but may not cause disease, infection may be asymptomatic
3) Persistent Latent - virus not detected in body fluids, hidden in a body part, viral genomes may spread extrachromosomally or enter host cell as proviruses, virus can be reactivated later in life as shingles
eg. following chicken pox, the virus remains latent inside trigeminal nerve ganglia
4) Persistend chronic - detected in body fluids at all times eg. Hep B

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6. Discuss the relationship of oncogenic viruses and human cancers

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Oncoviruses alter chromosomes of infected cells and transform them into tumor cells

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7. Describe virus replication cycle and its clinical significance

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6 steps of viral multiplication cycle:
1) Adsorption - virus attaches to host cell by binding of spikes to cell receptors
2) Penetration - virus engulfed into vesicle by endocytosis
3) Virus envelop uncoated - freeing viral genome into cell cytoplasm
4) Replication - under control of viral genes, cell synthesizes components of new viruses
5) Assembly - viral spike proteins inserted into cell membrane for viral envelope, nucleocapsid formed
6) Release - enveloped viruses bud off cell membrane, this complete virus is ready to infect another cell

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Term for the Study of Viruses

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Virology

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ANTIVIRAL AGENTS

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Interfere with steps in viral reproduction:
1) Entry/Release Inhibitors
eg. fuzeon, amantidine, tamiflu, relenza
2) inhibition of nucleic acid synthesis
eg. acyclovir, nevirapine
3) inhibition of effective assembly
eg. norvir, fortovase, rifampicin

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VIRAL ENVELOPE STRUCTURE

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External membrane containing lipoproteins enclosing capsid. More susceptible to chemical biocides (disinfectants) than non-enveloped viruses.

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DIFFERENCE BETWEEN VIRUS AND BACTERIA

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1) acellular vs cellular
2) virus is smaller
3) virus lacks independent mechanisms to metabolize, generate energy, multiply
4) obligate intracellular
5) one virus infects one sp only eg. polio viruses infects only humans

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TWO TYPES VIRAL STRUCTURE

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Naked, Enveloped

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CAPSID

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protein coat protecting viral genome

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GLYCOPROTEIN SPIKES

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On surface of envelopes. Allow attachment of virus to specific host cell surface receptor

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DNA VIRUSES

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Herpes Simplex Virus Type 2 (HSV-2) -genital herpes
-herpesviridae family
Hepatitis B
-hepadnaviridae family
Human Papilloma Virus (HPV)
Adenovirus
Parovirus B19
-infection during 1st trimester causes miscarriage
Smallpox
-Poxviridae family

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RNA VIRUSES

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Influenza
Respiratory Syncytial Virus (RSV)
-paramyxoviridae family
Severe Acute Respiratory Syndromes (SARS) Coronavirus
Rhinovirus (common cold)
-picornaviridae family
Norovirus (Norwalk)
Rotavirus
Hepatitis A Virus (HAV)
Human Immunodeficiency Virus (HIV)
-Acquired Immunodeficiency Syndrom (AIDS)
Coxsackie Virus B (myocarditis)
-picornaviridae family

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CONCENTRATION OF BLOOD COMPONENTS DURING HIV INFECTION

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1) HIV virus levels are high during initial acute infection (2months), decrease until later phases of hiv/aids
2) Antibody levels gradually rise and remain high
3) T-cell numbers remain relatively normal until later phases of HIV and full blown AIDS