VIRUS

VIRUS diverse

structure

genome

transmission host
algae
animal plants

replication
bacteria

mycoplasma

 Basis of Classification
1. 2. 3. 4. 5. 6. 7. Virion morphology Virus genome properties Physicochemical properties of the virion Virus protein properties Genome organization and replication Antigenic properties Biologic properties

A system has been established in which viruses are separated into major groupingscalled familieson the basis of virion morphology, genome structure, and strategies of replication

Yrs 2000 International Committee on Taxonomy of Viruses

4000 animal / plant viruses

56 families

9 subfamilies

233 genera

Hundreds unassigned

24 families

infect

animal & human

Chemical Composition of Viruses

Viral Protein Viral Nucleic Acid Viral Lipid Envelopes Viral Glycoprotein

Viral Lipid Envelopes

Viral Pathogenesis
Interaction of viral and host factors that leads to disease production.

Pathogenic Vilurent

Pathogenesis of Viral Diseases

STEPS

Entry and Primary Replication

Pathogenesis of Viral Diseases

STEPS

Viral Spread and Cell Tropism

 Viruses tend to exhibit organ and cell specificities. Tropism determines the pattern of systemic illness produced during a viral infection.
specific cell surface receptors factors affecting viral gene expression

Pathogenesis of Viral Diseases

STEPS

Cell Injury and Clinical Illness

Pathogenesis of Viral Diseases

STEPS

Recovery from Infection

Pathogenesis of Viral Diseases

STEPS

Virus Shedding

Host Immune Response

inhibit viral growth

mononuclear cells (T lymphocyte) neutralizing antibody (i.e. : IgA)

Viral Persistence
Chronic infections Latent infections Inapparent or subclinical infections

Acute Viral Respiratory Infections

Viral Infections of the GI Tract

herpes simplex virus and Epstein-Barr virus infect cells in the mouth. Acute gastroenteritis Rotaviruses, Norwalk viruses, and caliciviruses. Enteroviruses, coronaviruses, and adenoviruses often asymptomatic. Polioviruses, and Hepatitis A virus systemic disease, but no intestinal symptom.

Viral Skin Infection

Infected by:
Abrasion Arthropod vector Infected vertebra host Blood transfusion, tattooing, acupuncture

Lesion: macule, papule, vesicle, pustule Local/systemic

Viral Infections of the CNS

INFECTION
Bloodstream

growth through the endothelium of small cerebral vessels passive transport across the vascular endothelium

passage through the choroid plexus to the CSF

Neuronal

by transport within infected WBC

Congenital Viral Infections

Principals:
1. the ability of the virus to infect the pregnant woman and be transmitted to the fetus; the stage of gestation at which infection occurs; and the ability of the virus to cause damage to the fetus directly, by infection of the fetus, or indirectly, by infection of the mother resulting in an altered fetal environment (eg, fever)

2. 3.

Vaccine
utilize the immune response of the host to prevent viral disease. effective at reducing the incidence of viral disease. most cost-effective method of prevention of serious viral infections. Immunity immune response to specific antigen/glycoprotein on the surface of virus particle.

Vaccine

Killed-virus Vaccine
Advantage no reversion to virulence by the vaccine virus and that vaccines can be made when no acceptable attenuated virus is available. Disadvantages apply to killed-virus vaccines:
1.
2.

3.
4. 5.

Extreme care is required in their manufacture to make certain that no residual live virulent virus is present in the vaccine. The immunity conferred is often brief and must be boosted, which not only involves the logistic problem of repeatedly reaching the persons in need of immunization but also has caused concern about the possible effects (hypersensitivity reactions) of repeated administration of foreign proteins. Parenteral administration of killed-virus vaccine, even when it stimulates circulating antibody (IgM, IgG) to satisfactory levels, has sometimes given limited protection. The cell-mediated response to inactivated vaccines is generally poor. Some killed-virus vaccines have induced hypersensitivity to subsequent infection, perhaps owing to an unbalanced immune response to viral surface antigens that fails to mimic infection with natural virus.

Attenuated Live-Virus Vaccines

Advantage acting like the natural infection with regard to their effect on immunity. Disadvantage:
1.
2.

3. 4.

The risk of reversion to greater virulence during multiplication within the vaccinee. Although reversion has not proved to be a problem in practice, its potential exists. Unrecognized adventitious agents latently infecting the culture substrate (eggs, primary cell cultures) may enter the vaccine stocks. Viruses found in vaccines have included avian leukosis virus, simian polyomavirus SV40, and simian cytomegalovirus. The problem of adventitious contaminants may be circumvented through the use of normal cells serially propagated in culture (eg, human diploid cell lines) as substrates for cultivation of vaccine viruses. The storage and limited shelf life of attenuated vaccines present problems, but this can be overcome in some cases by the use of viral stabilizers (eg, MgCl2 for poliovaccine). Interference by coinfection with a naturally occurring, wild-type virus may inhibit replication of the vaccine virus and decrease its effectiveness. This has been noted with the vaccine strains of poliovirus, which can be inhibited by concurrent infections by various enteroviruses.