1. Pathogenic Viruses
Name of virus; what family it belongs to; what disease it causes.
DNA or RNA? Ss or ds?
Characteristics of disease, symptoms.
Viral virulence factors
Epidemiology: reservoirs, vectors
Immunizations

2. Brief review Non-cellular “life forms”
Consists of nucleic acid and capsid (protein)
Some types possess envelope, spikes, accessory proteins
Obligate intracellular parasites
Nucleic acid enters host cell, directs operations
Ultimately, new copies of viral N.A., proteins made
Virus depends mostly on host cell machinery
Following assembly, new virions escape to infect new hosts

3. Attack and defense Virus has ways of attacking
Specific binding to host cell receptor
Receptors involved in normal cell functions
Virus may regulate cell division for its own replication
Insertion of viral DNA into chromosome allows virus to hide from immune system
Causes adjacent cells to fuse, allows cell to cell spread without leaving cell.

4. Defense by host Host has ways of defending
Cell mediated immunity (T cells): infected cells killed.
Antibodies intercept virions between cells, in fluids
Interferon produces anti-viral state, prevents replication

5. Our selections for Fall 2005
Herpes Virus family
HSV 1 & 2; VZV; EBV, and CMV
Hepatitis viruses
Hep A, B, and C.
Mosquito-borne viruses of Arkansas
Picornaviruses and common cold viruses
Influenza
HIV and sexually transmitted viruses
Sort of a mixture of groupings by type and groupings by disease.

6. Herpes virus family Human herpes viruses now numbered As a family:
But common names easier to use.
As a family:
ability to become latent;
predilection for either nervous tissue or lymphocytes;
ability to cause cancer.
Herpes roster:
Herpes simplex, Varicella zoster, cytomegalovirus, Epstein Barr, roseola, Kaposi’s sarcoma virus.

7. Herpes Simplex viruses
HHV1 (above the waist)
Typically oral, cold sores; flu-like symptoms, etc.
HHV2 (genital), STD and neonatal
Painful, contagious sores on genitals, overlap w/ HHV1.
Latency
Viruses enter nearby nerve cells, remain until activated by stress of some sort, cause disease, then return.
Spread and treatment:
Person to person by direct contact; spread within host by forming syncytia, escape immune system.
Acyclovir helps; no cure, lifetime infection.

8. Herpes family: Varicella Zoster
Varicella: chicken pox; Zoster: shingles
Chickenpox (not a pox virus), respiratory, disease becomes systemic with fever, malaise, skin lesions.
Very contagious; usually mild, esp. in children
Virus can become latent in nerves like Herpes simplex
Recurrence: shingles; rash, pain, on one side
Acyclovir can lessen symptoms
Beware of salicylates + viruses: Reyes syndrome
Vaccination: Varivax: attenuated vaccine

9. Note how rash does not cross the midline.
Shingles
Note how rash does not cross the midline.
Shingles occurs most frequently on the trunk, but a Google search shows pictures of face, legs, etc. as well.

10. Herpes family: Cytomegalovirus
CMV (HHV5): Infection results in enlarged cells
Widespread asymptomatic infections, latency
Virus shed in body fluids: sex, birth, transplants
Problem for unborn, immunosuppressed, transplant patients; major cause of viral-induced birth defects.
Rubella, a togavirus, was once the major viral cause of birth defects.

11. Epstein-Bar Virus Cause of infectious mononucleosis
Infects B cells and salivary glands
Spread by respiratory droplets, kissing
Sore throat, swollen glands and spleen
Long lasting fatigue
Lympho-civil war: cytotoxic T cells attack infected, altered B cells.
Same virus causes B cell cancer (Burkitt’s lymphoma) in Africa
Some relationship to malaria exposure

12. Hepatitis Hepatitis is inflammation of the liver
Liver especially important in metabolism
Breakdown of drugs, toxins, waste products
Damage results in accumulation of bilirubin
Bilirubin is a stage in hemoglobin breakdown
Results in yellow color: jaundice
Hepatitis can be caused by several different viruses
Hepatitis A, B, and C viruses all cause liver damage, but are unrelated viruses.

13. Hepatitis B A DNA virus: “Hepadnavirus”
Hepatitis B released from live cells, so accumulates in high numbers in body fluids.
Blood of infected person is rather infectious
Cuts, piercing, sex, childbirth, etc.
Large amounts of empty capsids ties up antibodies.
After exposure, long incubation, long disease
10% have chronic infections
The younger the host, the likelier chronic infection

14. Hep B continued Chronic infection correlated with liver destruction
Liver tissue replaced by scar tissue; liver failure
Long term exposure to virus increases risk of liver cancer
Insertion of HBV DNA into chromosome may activate oncogenes
Vaccination now recommended
Because of bad result of early infection and great danger of liver damage, liver cancer.
Recombinant vaccine.

15. Hepatitis A virus A small RNA virus, “Picornavirus”
Transmitted by fecal-oral route
Incubation for 1 month, followed by fever, nausea, anorexia, jaundice
T cells attack infected liver cells
No chronic infections, patients recover.
Note comparisons to Hepatitis B:
RNA vs DNA
Shorter disease, few long term problems
Mode of spread completely different

16. Hepatitis C Another RNA virus, different group: “Flavivirus”
Causes chronic infections >80%
Often mild with few symptoms until damage
Long period between infection and damage
Long term infections increase risk of cancer.
Transmission like Hep B: blood, sex, transplants