Module 9: Virus Biology

Properties of viruses

not cells, cannot make proteins; infectious particle; can be active/inactive not dead/alive; obligate intracellular agents

Obligate intracellular agent

multiplies only in the host cell, instruct cell to make and release new viruses

Viral shape and size

smaller than most bacteria

Viral component

only need parts needed to invade and control host cell: external coating and core containing nucleic acids

Capsid

Protective shell around the nucleic acids, made of capsomeres

3 types: helical, icosahedral, prolate

Nucleocapsid

the capsid and nucleic acid

Capsomeres

identical protein subunits, spontaneously self assemble

Helical capsid

rod-shaped capsomeres form a continuous helix around nucleic acid; can be naked or enveloped

Naked virus

nucleocapsid only

Enveloped virus

has an envelope around nucleocapsid

Icosahedral Capsid

3-D, 20 sided figure with 12 evenly spaced corners, naked or enveloped

Prolate Capsids

Bacteriophages, multiple protein types, docks to the bacteria with tail fibers, penetrate bacteria using tail pins

Spikes

allow for docking with the host cell, made of glycoproteins

Virion

fully formed virus that is infective

Envelope

composed of host membrane; host membrane proteins replaced with viral proteins, contains spikes

Viral genome

small and simple genomes, can be linear or circular, 1 molecule segment, DNA or RNA, single stranded or double stranded

Viral life cycles

2 types: enveloped RNA animal virus and Phage

Bacteriophage

also known as phage; bacterial virus

Receptors

protein molecules on surface of cells, can be enzymes, receives signals from outside which causes action inside, virus spikes bind to these receptors(very specific)

Enveloped RNA animal virus life cycle

Adsorption→Penetration by endocytosis→uncoating after endocytosis→synthesis→assembly→release of mature viruses

Host range

virus can invade its host only by making an exact fit with a specific host receptor; can be restricted, intermediate, or broad

Restricted host range

Hepatitis B→bind only to human liver cells

Intermediate host range

Poliovirus→bind to primate intestinal and nerve cells

Broad host range

Rabies virus→bind to various cells of all mammals

Adsorption

Virus encounters susceptible host and adsorbs specifically to receptors on host cell membrane(spikes binds to receptors); limits host range

SARS-CoV-2 binding

spikes bind to ACE2, an enzyme attached to cell membranes in lungs, arteries, heart, kidney, and intestines

Penetration by endocytosis

virus is engulfed by the cell and enclosed in a vacuole or vesicle

Uncoating after endocytosis

enzymes in the vacuole dissolve envelope and capsid; virus is released into the cytoplasm

Synthesis

viral nucleic acid takes control of host’s synthetic and metabolic machinery→production of viral RNA, capsomeres, and spikes

Assembly

viruses built from growing pool of parts→viral spikes added to host membrane then become part of viral envelope

Release of mature viruses

also known as viral budding or exocytosis; nucleocapsid binds to inside host membrane→pouch formation→pouch pinched off, virus released with envelope→viruses shed gradually, no cell destruction

Bacteriophages

viruses that infect every known bacteria species, very host specific, and often make host more pathogenic to humans

Phage life cycle

type 1- lytic cycle or type 2- lysogenic phase

Lytic cycle

ends in host cell death; cell lysis releasing virions, virulent phage

Lysogenic phase

no immediate replication and lysis, undergo adsorption and penetration then DNA incorporated into host genome, then waits(temperate phage); host DNA replication causes viral DNA also to be replicated

Prophage

inactive; phage DNA is part of host chromosome

Induction

prophage activation→lytic cycle

Lysogeny in human disease

some phage genes code for toxins which can cause human pathology

Lysogenic conversion

acquisition of new traits by bacteria from temperate phage, virus genes get stuck in bacteria host, such as cholera and botulism toxin

Cytopathic effects(CPE’s)

virus-induced cell damage that alters its appearance; cells become disoriented, undergo major changes in shape/size, and intracellular damage; inclusion bodies and syncytia

Inclusion bodies

compacted virus masses or cell damage

Syncytia

fusion of multiple host cells into 1 large cell with multiple nuclei, used to identify viral infections

Oncogenic viruses

cause cancer, 20% of human cancers

Transformation

effect on cell caused by oncoviruses; causes faster and indefinite cell division, chromosome alteration, and changed cell surface molecules

Viral nucleic acids

used to classify viruses with the Baltimore System

4 types: DNA, RNA, double stranded, and single stranded

Retroviruses

some RNA viruses; uses reverse transcriptase to convert viral RNA to viral DNA, DNA incorporates into host genome, becomes provirus

Double stranded DNA viruses

cow pox, small pox, herpesviridae, and human papillomavirus

Cow Pox

causes pustules, zoonotic(cows, dogs, etc), transmitted by casual contact

Small Pox

causes scarring, blindness, limb deformities; transmitted by contact/inhalation; 30-80% mortality, eradicated in 1977

Herpesviridae

4 types: HSV-1, HSV-2, HSV-3, HSV-4

HSV-1

causes fever blisters and cold sores, transmitted by saliva usually during childhood, 95% of people infected

HSV-2

genital herpes, transmitted as STD or by skin contact

HSV-3

varicella-zoster virus; causes pustules, transmitted by casual contact, complicated cases can be treated

HSV-4

Epstein-Barr virus, infectious mononucleosis, kissing disease; causes fever, fatigue, inflamed throat, swollen lymph nodes, cancer(lymphoma); transmitted by saliva/genital secretions

Human papillomavirus

causes warts, asymptomatic, infects skin and mucosal epithelium, enters cuts

vaccine for HPV which prevents types causing cervical cancer