Chapter 6: viruses and other acellular infectious agents

viruses

• protein and nucleic acid

• acellular infectious agents that can’t reproduce outside of living cells

• infect all types of cells but specific for certain organisms

  • ex: bacteriophages (phages) infect bacteria

viroids

• only RNA

• circular ssRNA molecules that lack a capsid and cause a variety of plant diseases

  • do not act as mRNAs and appear to be replicated by host RNA polymerases

virusoids

• only RNA

• circular ssRNA molecules encode proteins and need helper viruses for infectivity

• hepatitis D requires the help of the hepatitis B virus

prions

• proteins only

• proteinaceous infectious praticles (prP) are not associated with nucleic acid genome

  • PrP has been identified in normal animal tissue

  • abnormal PrP causes prion diseases by inducing a conformational change of the cellular PrP to the abnormal form

• cause progressive, degenerative CNS disorders

  • ex: scrapie (sheep and goats)

  • ex: bovine spongiform encephalopathy (mad cow disease)

  • ex: kuru (cannibalism)

  • ex: fatal familial insomnia

  • ex: Gerstmann-Strassler-Scheinker

  • ex: Creutzfeldt-Jakob disease (CJD)

structure of viruses

• size: 10 nm to 300 nm

• nucleocapsid

• three types of capsid symmetry:

  • icosahedral (geometric)

  • helical

  • complex (mix or icosahedral and helical)

• capsids are constructed from many copies of one or a few types of proteins and assembled together with the viral genome

• enveloped and nacked viruses

nucleocapsid

nucleic acid plus surrounding capsid (protein coat that surround genome)

• this might be the whole virion for some viruses, others may just posses structures

enveloped viruses

have an outer membranous layer

naked viruses

viruses that lack an envelope

viral envelopes and enzymes

• envelopes are membrane structures surrounding some viruses

  • lipids and carbohydrates derived from the host membranes

  • proteins are virus-specific

  • many have glycoprotein spikes (peplomers)

    • ex: enzymes neuraminidase and hemagglutinin

• lack true metabolism → carry one or more enzymes that are involved in viral nucleic acid replication

  • enzyme can be capsid-associated, or it can be located within the capsid

• viral genomes are either RNA or DNA → single or double stranded

  • most common is dsDNA and ssRNA

virus multiplication

• adsorption: attachment to the host cell

  • entry of a nucleocapsid or viral genome into the host cell

• synthesis stage: expression of viral genes in the host cell

  • virus takes control of the cell’s machinery and produces viral proteins and genomes

• new virions self-assemble into mature virions

• virions released by budding or cell lysis

types of viral infections: bacterial and archaeal cells

• lysis and lysogeny

• virulent phages

• temperate phages

virulent phages

• only capable of the lytic cycle

  • where multiplication begins once entering the host and continues until the host lyses

temperate phages

• : capable of lysogeny, nonlytic relationship with their hosts

  • virulent phages lyse their hosts in addition to the lytic cycle

• lysogenic viral genome (prophage): remains in the host but does not kill the host cell → lysogenic (lysogens)

  • switch to the lytic cycle at some later time (induction)

infection of eukaryotic cells

cytocidal infections

cytocidal infections

• lead to cell death

• some viruses persist in the host for many years

  • in some cases, degenerative changes occur in cells without causing lysis

epstein-barr virus on eukaryotic cells

burkitt’s lymphoma nasopharyngeal carinoma

hep B virus on eukaryotic cells

hepatocellular carinoma

hep C virus on eukaryotic cells

hepatocellular carinoma

human herpesvirus 8 on eukaryotic cells

kaposi’s sarrcoma

human papillomavirus on eukaryotic cells

cervical cancer

HTLV-1 on eukaryotic cells

leukemia

viruses and cancer

• a disease where there is abnormal cell growth → neoplasia

• spread of the abnormal cells throughout the body → metastasis

pathogenicity of viroids

• results from RNA slicing, where viroid RNA forms dsRNA by pairing with host mRNA’s

• dsRNA are destroyed by host cell defenses and hence certain host gense are not translated → disease