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

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

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.

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

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.

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.

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.

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

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. http://www.irishhealth.com/content/image/1191/shingles.jpg

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.

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

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.

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

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.

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

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