Herpes Viruses

Introduction
All herpes viruses can develop a latent state within specific tissues, in which they rest until reactivation. Reactivation is triggered by menstruation, anxiety states, fever, sunlight exposure, or weakening of the immune system. Viruses cause cells to become multinucleated giant syncytial cells with intranuclear inclusion bodies, and cause local destruction when they migrate to the peripheral skin. Disease is resisted by cell-mediated immunity, but the virus remains latent in nerve cells throughout one's life.

Only alpha subfamily viruses (herpes simplex 1 and 2, and varicella zoster) cause cell damage to the skin.

Herpes simplex virus 1 & 2
Latent in nerve cell bodies. HSV-1 produces most cold sores and HSV-2 produces most genital herpes. Symptoms include watery blisters in the skin or mucous membranes of the mouth, lips or genitals. Herpes simplex can be spread through contact with saliva. HSV infection during pregnancy can result in transplacental viral transfer (by crossing the blood-placenta barrier).

Varicella zoster virus 
Latent in nerve cell bodies. Causes varicella (chickenpox) AND herpes zoster (shingles). A breakout of shingles causes painful skin rashes.

Cytomegalovirus
Latent in salivary glands, and dendritic and myeloid cells. CMV infects both epithelial cells and various cells of the immune system. Infection is typically unnoticed in healthy people, but can be life-threatening for the immunocompromised. CMV causes four infectious states: (1) Asymptomatic (2) Congenital disease in infants by transmission from mother, causing mental retardation (3) Mononucleosis syndrome in young adults (4) Reactivation, causing retinitis (blindness), pneumonia or disseminated infection.

Epstein-Barr virus
Latent as multiple copies of circular DNA. Causes mononucleosis by infecting B cells, and is involved in certain cancers. EBV causes cells to "transform" and act as cancer cells, passing on copies of EBV DNA to their progeny. However, malignant cells are cleared by the immune system, with the resolution of mononucleosis illness.

Hepatitus Viruses

Introduction
There are five main hepatitis viruses (types A, B, C, D and E) that infect the liver. F and G are not considered to be dangerous. Only hepatitis B (and hepatitis F) viruses are DNA viruses; the remaining types are RNA viruses. All hepatitis viruses are parenteral transmission except for A and E, which are fecal-oral transmission.

Symptoms
Acute (lasting fewer than 6 months)
Initial non-specific flu-like symptoms. May include fatigue, fever, headache, muscle and joint aches, coughing, vomiting, and diarrhea. Many hepatocyte death results in the release of high levels of cell enzymes AST and ALT. Some pericanalicular (bile duct lining) cell death results in low levels of GGT and alkaline phosphatase. The presence of these enzymes in the blood is a sign of hepatitis.

As the liver swells, the bile duct becomes blocked, causing a backup of bilirubin to the blood. In 1-2 weeks, the buildup of bilirubin leads to jaundice due to the liver's failure to metabolize and excrete bilirubin.

Chronic
Often asymptomatic, with enlarged liver and mildly elevated liver enzyme levels in the blood. A first-time, acute hepatitis infection can become chronic if the virus is not cleared in 6 months.

HAV
Frequently affects young children. Transmitted by fecal-oral route from poor hand washing, or from ingesting contaminated water.

HBV
Virus lives in all fluids of an infected patient. Transmitted by blood and sexual contact. Only 10% develop chronic hepatitis.

HCV
Leading cause of chronic hepatitis in the United States. 85% develop chronic hepatitis from acute infections. Transmitted parenterally primarily via injections from drug use.

HDV
Replicates only with the help of HBV by using the envelope of HBV to cause infection. An HDV infection to a chronic HBV carrier results in severe acute hepatitis. As carriers can't make antibodies against HBV, they also become carriers of HDV.

HEV
Similar to HAV. Endemic to Asia, India, Africa, and Central America.

Influenza Viruses (Orthomyxoviridae and Paramyxoviridae)

Structure
Viruses are spherical, containing negative stranded RNA; outer membrane contains hemagglutinin activity (HA) and neuraminidase activity (NA) glycoproteins that are anchored to the inner lipid bilayer by M-proteins.

Hemagglutinin
Attachment to host cell sialic acid receptors, which are found on the surface of red blood cells, and upper respiratory tract cells. HA is needed for absorption of the viral genome.

Neuraminidase
Cleaves neuraminic acid of the mucin upper respiratory barrier to expose sialic acid receptors; also cleaves sialic acid receptor to avoid attachment of budding viruses, which will escape to infect new cells. 

In paramyxoviruses, HA and NA are part of the same glycoprotein spike. They also contain fusion protein (not found in orthomyxoviruses) that causes the infected cells to fuse into giant multinucleated cells.

Orthomyxoviridae
Orthomyxoviruses are influenza viruses, of which there are three types. Type A infects humans, other mammals, and birds, whereas type B and C infect only humans. Type A causes the most severe disease, with Type B and C in decreasing severity.

Paramyxoviridae (colds/flu in adults, pneumonia in children, measles, mumps)
Paramyxoviruses include parainfluenza viruses, respiratory syncytial virus (RSV), metapneumovirus, mumps virus, and measles virus.

Metapneumovirus causes upper and lower respiratory tract infections primarily in young children or elderly. Parainfluenza and RSV cause upper respiratory infections that have cold-like symptoms in adults, but produce influenza-like sickness from lower respiratory tract infections (bronchiolitis, viral pneumonia, croup) in children, elderly, and immunocompromised patients.