Medical student study aid - List of viruses by family and by type of disease caused. Viruses are color-coded and organized by syndrome. Treatment information is included where available when chart was made.

1. Disease Family Treatment Symptoms
Hepatitis A (HAV)
acute
 Fulminant hepatitis
Hepatovirus of
Picornaviridae
family, formerly
Enterovirus 72
(ss naked +RNA)
Diagnostic: serological tests,
time course of symptoms
and identification of source
Treatment: post-exposure
prophylaxis via passive
immunization with pooled
serum Ab; vaccination with
inactivated HAV can be
used pre or post-exposure.
Transmission via fecal-oral, often
due to contaminated food sources.
Characterized by fever, fatigue,
nausea, loss of appetite and
abdominal pain 15 to 50 days after
exposure. Icteric (liver damage)
phase and jaundice occur 4-6 days
after onset of symptoms.
Children often asymptomatic or have
mild symptoms.
Rapid onset of symptoms associated
with liver failure and encephalopathy.
80% mortality rate.
Hepatitis B (HBV)
acute
Hepadnaviridae
(ds enveloped
DNA)
Diagnostic: CPE - Dane
particles, Ig reactivity to
HB Ab, liver enzyme panel
Treatment: None 100%
effective. Alpha-interferon,
pegylated interferon via
injection. Oral nucleoside
and nucleotide analogues
block viral RTase -
lamivudine, adefovir,
dipivoxil, entecavir.
Hepatitis B immune
globulin (HBIG) after
exposure or IBIG and
vaccination for exposed
infants can prevent
infection.
Infection via exposure to blood and
body fluids (includes perinatal
transmission).Virus particles are
highly infectious and persist up to 7
days outside the body.
Produces chronic carrier condition
(mostly children) that can lead to
hepatocellular carcinoma or acute
clinical illness (mostly adults)
characterized by malaise, lethargy,
anorexia, pain in upper right quadrant
that can be followed by an icteric
phase of 4-8 weeks.
Liver pathology due to CMI response
via cytotoxic T lymphocytes.
Hepatocellular Carcinoma
(HCC)
HBV Cancer caused by increased cellular
division in virus-infected cells.
Hepatitis C (HCV)
 Acute hepatitis
 Chronic persistent
hepatitis
Flaviviridae,
family
Hepacivirus
(ss enveloped
+RNA)
Diagnostic: detection of Ab
via ELIZA, RT-PCR, liver
enzyme panel, persistent
detection of Ab and HCV
RNA
Treatment: alpha-interferon,
pegylated interferon and
ribavirin reduce viral
replication and liver damage
but do not clear infection.
Ab ineffective (symptoms
resolved before Ab is
produced)
Transmission primarily via
blood/fluids
Mean incubation: 8 weeks; presents
with fever, anorexia, nausea,
vomiting and jaundice. Virus
clearance and recovery
Most prevalent – no apparent
symptoms upon infection. Chronic
symptoms develop within 10-15
years and leads to cirrhosis.
Viral reproduction in liver leads to

2.  Cirrhosis
hepatocyte destruction via CMI.
Loss of liver function due to damage.
Hepatoma (also HHC) HCV RNA virus that does not carry
oncogene – slow transforming virus.
No DNA intermediate.
Hepatitis D (HDV)
 Superinfection
(superimposed D after
B)
Deltavirus
(ss enveloped
neg-sense RNA)
Diagnostic: Serology for
anti-HDAg Ab, delta Ag
and HDV RNA. HDV-IgG
will indicate persistent
infection.
Treatment: Alpha-interferon
may reduce symptoms.
Prevention: HBV vaccine
Infection only produced in cells
coinfected with HBV. Transmitted
via blood, sexually, and perinatally.
Incubation 3-7 weeks.
Liver damage caused by T-cell
mediated IR. Infection can become
persistent, chronic and lead to
cirrhosis, especially with
superinfection.
Hepatitis E (HEV) Hepevirus
(ss naked +RNA)
Diagnostic: no laboratory
diagnostics available,
diagnosis made by
excluding other hepatitis
viruses
No treatment, no vaccines
available
Presents with symptoms similar to
HAV but has higher mortality rates in
pregnant women. Does not cause
chronic infection.
Hepatitis G (GB-C) Flaviviridae,
genus Pegivirus
(ss enveloped
+RNA)
Diagnostic: serology for
anti-GB-C Ab, isolation of
virus
No vaccine
Chronic, long lasting infection
transmitted via sexual intercourse
and blood.
May interfere with HIV replication
and extend HIV patient lifespan.
Poliomyelitis
 Abortive poliomyelitis
 Aseptic meningitis
 Paralytic polio
Poliovirus
(Enterovirus)
Diagnostic: cell culture from
throat, stool or CSF sample
and neutralization by Ab,
detection of anti-polio Ab
Vaccines: Sabin (OPV) is
live attenuated virus and
Salk (IPV) is
killed/inactivated virus.
Treatment: Pleconaril
(limited availability) inhibits
viral penetration into cell;
supportive/symptomatic
Can be asymptomatic. Causes
permanent motor nerve damage.
Febrile illness, headache, malaise,
sore throat and vomiting within 3-4
days of exposure. (May present with
rash).
Nonparalytic type; spontaneously
resolves. Presents with stiff neck,
back pain (from CNS/meninges
entry) and muscle spasms in addition
to febrile illness.
Most severe form; biphasic illness
where paralysis of muscles appears 3-
4 days after minor illness (virus kills
motor neurons of anterior horn of
spinal cord).

3.  Bulbar poliomyelitis
 Post-polio syndrome
Paralytic polio affecting brain stem
and resulting in respiratory paralysis;
potentially life threatening.
Acute deterioration of residual
function of affected muscles years
after initial polio infection. Cause
unknown.
Coltivirus
 Colorado Tick fever
 Salmon River virus
Coltivirus of the
Reoviridae family
Diagnostic: blood tests to
confirm infection –
complement fixation,
immunofluorescence, CBC,
liver enzyme panel and
creatine phosphokinase
Treatment: symptomatic
Transmitted by adult female hard-
shelled wood tick. Common in
western US and Canada (high
elevations).
3-6 days after bite, presents with
diphasic fever, severe headache,
weakness, muscle aches,
nausea/vomiting, rash, photophobia,
hepatosplenomegaly possible.
No info provided.
Gastroenteritis, “stomach
flu”
 Rotavirus Group A
 Atypical rotaviruses (B
and C)
 Human astrovirus
Reoviridae
(respiratory
enteric orphan)
Reoviridae
(respiratory
enteric orphan)
Astroviridae
Diagnostic: stool sample
analyzed for Ag (EIA or
Latex IA) or Ab (4x titer)
Treatment is symptomatic
and involves replacement of
fluid and electrolytes.
Prevention by hygienic
measures: hand washing,
isolation of infected
patients, proper disposal of
enteric wastes. (Infective
dose is low.)
2 live attenuated
multivalent rotavirus
vaccines available.
Diagnostic: stool sample
detection via immunoassay,
dot blot hybridization.
Prevention: good hygiene
Treatment: supportive
One of the most common infections
seen by physicians. Diarrhea is a
significant worldwide cause of death,
especially for malnourished.
Infection via ingestion of material
contaminated with feces (oral-
fecal). Replication requires GI
protease.
Primarily infects enterocytes of small
intestine villi, reducing water
absorption and inducing toxin-
mediated intestinal fluid secretion.
CMI and Ab important for immunity.
Most infections caused by this
subtype; usually infects 6 – 24 month
olds. 90% have Ab by 3 Y.O.
Less common. Group B 
waterborne outbreaks in China.
Group C in pigs and occasionally
infects humans.
Minor cause of gastroenteritis. Host-
specific virus that infects mainly
children and elderly; can be seen with
AIDS. Peaks cooler months.
Most adults have Ab.

4.  Norovirus
 Enteric adenoviruses
(subgroup F, serotypes
40, 41)
Caliciviridae
(Sapovirus from
same family and
generally the
same as
norovirus)
Adenoviridae
(naked linear ds
DNA, 5’ protein,
icosahedral)
Diagnostic: stool sample
analysis via PT-PCR but not
usually performed since
recovery occurs within 24
hrs. Human strains cannot
be cultured.
Treatment: supportive;
replenish fluids and
electrolytes.
Prevention: Low infectious
dose and high levels in
stool = spreading easily.
Good hygiene best
preventative. Alcohol-based
hand sanitizers not
effective.
No vaccine available.
Cell culture difficult to
impossible.
Environmentally stable; incubation
period 24-48 hrs. Oral-fecal infection,
usually in confined populations.
“Winter vomiting disease” Airborne
spread via vomitus particles or more
commonly spread via contaminated
foods.
30% asymptomatic. Presents with
acute-onset nausea and vomiting,
abdominal cramps, watery diarrhea
and sometimes low fever.
Dehydration most common
complication and vomiting more
common in children. Causes
destruction of villi cells. Attachment
mediated by HBGAs.
Second to rotavirus in causing acute
diarrhea in children. Infections occur
year-round but peak in warmer
months.
Coxsackie A
 Herpangina
 Hand-foot-and-mouth
disease
Coxsackie B (body)
 Pleurodynia
 Myocarditis/Pericarditis
Coxsackievirus Diagnostic: Cell culture,
then immunofluorescence,
ELIZA, RT-PCR, Ab titer
No vaccine and no specified
treatment
Infects via skin and mucous
membranes via respiratory aerosols
(fecal-oral).
Self-limiting fever, sore throat, tender
vesicles in oropharynx, anorexia,
vomiting
Self-limiting vesicular rash on hands
and feet, ulcerations in mouth, mild
fever; occurs mainly in children
Causes visceral disease. B4 linked to
diabetes in humans.
Fever and severe pleuritic/lung chest
pain (devil’s grip)
Fever, chest pain, congestive failure
that is most serious in newborns; can
lead to serious heart damage/failure

5. Rhinovirus (HRV)
 Species A
 Species B
 Species C
Enterovirus in the
picornavirus
family
(ss linear naked
icosahedral
+RNA)
Diagnostic: clinical and
epidemiological criteria.
Isolation requires testing of
nasal secretions. Serology is
of little use.
Prevention: hygiene and
disinfecting surfaces.
Treatment is symptomatic.
Antivirals hindered by drug
resistance.
No vaccine due to > 100
serotypes
Cause of most respiratory tract
infections (common cold). Infects
epithelial cells of nasopharynx via
ICAM binding. Transmission is often
by hands via aerosols and droplets
(nasal secretions). Large droplets
infective up to 5 days. Incubation up
to 7days and communicable from 24
hrs before to 5 days after onset.
Present with little or no fever, red
nasal mucosa, rhinorrhea, headaches,
cough, malaise, chills. Rarely spreads
to LRTI.
More frequent in children and
prevalent in early fall to late spring.
Echovirus Echovirus Diagnostics: Cell culture;
serological tests not helpful
No antivirals, no vaccines.
URTI, febrile illness with or without
associated rash, hemorrhagic
conjunctivitis. Can cause aseptic
meningitis.
Causes diarrhea in infants.
Coronavirus
 HCV-229E
 HCV-OC43
 HCV-NL63
 HCV-HKU1
 SARS-CoV
Coronaviridae
(ss linear
enveloped +RNA)
Diagnostic: Can be
identified by appearance of
“halo” due to protruding
spike protein.
No real treatment, no
prophylaxis, produces poor
acquired immunity, no
cross-immunity,
No vaccines available.
Diagnostic: 2+ times PCR
analysis of 2 different
specimens (stool, nasal,
etc.), seroconversion via
ELIZA/IFA with 4x titer
between phases.
Prevention: Isolation/
quarantine, PPE with N95
mask, report confirmed
cases to WHO.
Treatment: corticosteroids
for lung inflammation,
antivirals (Ribavarin) and
antibiotic to prevent
secondary infections,
supportive therapy.
Second leading cause of RTIs. Most
common in children. Incubation 2-5
days. Infections peak in winter- early
spring with epidemics every 2-4 yrs.
“Common cold syndrome,” no
viremia, usually => URTI, slow,
patchy destruction of ciliated
epithelial cells and loss of beating
cilia. Typified by nasal discharge and
malaise.
Transmitted by close contact via
aerosol, droplets and fecal-oral.
Uses ACE2 enzyme and establishes
URTI that can spread to GI, liver,
kidney or brain.
Alveoli have influx of macrophages
and giant multinucleated cells
(syncytia).
Presents as an atypical pneumonia:
sudden onset of high fever, muscle
aches, headache, sore throat, dry
cough and may require mechanical
ventilation. Lymphopenia and
elevated liver enzymes associated;
chest x-rays show infiltrates.
Symptoms occur while titers low.
Pandemic

6. Human enteric coronavirus Torovirus
Parainfluenza Virus
 PIV1
 PIV3
 PIV2
 PIV4a
 PIV4b
Paramyxoviridae
(Respirovirus)
Paramyxoviridae
(Rubulavirus)
Diagnostic: croup diagnosed
on H&P findings (barking
cough) and X-rays.
Viral Ag detection on
nasal/throat samples rapid
but has low sensitivity.
Serology detects IgM, IgG
or Ab. PCR useful for PIV-3
detection.
Treatment: Supportive -
decongestants, steam,
oxygen and intubation if
needed. Racemic
epinephrine reduces
airway obstruction. Treat
bacterial complications as
they occur. Contact
precautions.
No vaccines available.
Spreads by droplet and rarely
produces viremia. Incubation 33-6
days and reinfections are common
due to multiple serotypes.
Cause URTI in adults. May progress
to LRTI in children/infants.
Lymphocytosis possible.
Complications include parotitis,
meningitis, and encephalitis.
Produces more severe infection.
URTI. Commonly causes infant
croup. Peaks in fall (biannual).
Pneumonia and bronchiolitis
common. Infections peak in spring
and summer.
Produces less severe URTI but can
lead to infant croup with fever,
cough, stridor, and respiratory
distress. Infects larynx. Peaks in fall,
sporadic.
Usually produce asymptomatic
infection.
Mumps Paramyxoviridae
(Rubulavirus)
Diagnostic: clinical
diagnosis via enlargement of
salivary glands. Serology
effectively detects IgM.
Only one serotype. Virus
can also be isolated from
saliva, urine and CSF using
ELIZA/IF or
hemagglutination.
Treatment: No antivirals
available. Droplet
precautions.
Vaccine: live attenuated,
MMR and MMRV, 2 doses.
Incubation: 16-18 days. Prevalent late
winter-spring. Moderately
contagious infection of the parotid
glands producing inflammation with
swelling behind ears and difficulty
swallowing. Transmitted via
respiratory secretions and
replicates in upper respiratory
tract/lymph nodes before viremia.
30% of infections are
asymptomatic. Meningitis, CNS
involvement common. May infect
pancreas, ovaries, heart or kidney.
Complications include encephalitis,
deafness, and orchitis (post-pubertal).

7. Respiratory Syncytial Virus
(RSV)
Paramyxovirus
(Pneumovirus)
Diagnostic: One serotype.
Cell culture with IF on
exfoliated cells or ELIZA
after PCR of mucus sample.
Physical findings of RSV
bronchiolitis – nasal flaring,
expiratory grunt, prolonged
expiration, rales, chest wall
retractions, tachypnea and
apnea.
Treatment: Ribavirin
(guanosine analog) for
severe illness, Palivizumab
(Ab) against F protein
given monthly to
premature infants.
Supportive with oxygen,
bronchodilators, respiratory
support as needed. Contact
precautions.
Vaccine: None available.
Previous vaccines have
aggravated illness.
Most important respiratory
pathogen in children. Major cause
of bronchiolitis and pneumonia in
infants. Most common infectious
cause of death in first year.
95% of children have Ab by age 5.
Most common in infants ages 2-6
mos. Incubation: 11 days. Peaks
winter and spring. Highly contagious
and nosocomial infection common.
No lasting immunity. Reinfections
limited to URTI.
Adults: URTI; causes severe disease
in elderly (2nd
to influenza).
Infants: LRI (bronchiolitis); usually
starts with 2-3days of URTI
progressing to LRTI. Presents with
cough, wheezing, anorexia, emesis,
respiratory distress, and sometimes
hypoxemia present. No wheezing
during tachypnea is ominous sign in
infant.
Human metapneumovirus
(hMPV)
Paramyxovirus
(Pneumovirus)
Contact precautions Resembles RSV but usually infects
older individuals. A leading cause of
bronchiolitis in infants. Prevalent late
winter-early spring.
Present with high fever, cough, sore
throat, and coryza. May have
bronchiolitis.
Influenza Orthomyxoviridae Diagnostic: RT-PCR and
rapid test (for Ag) for types
A and B.
Treatment: Antivirals
reduce duration and
complications but must be
administered within first 24-
48 hours of onset.
 Neuraminidase
inhibitors prevent
virion release for type
A & B. Zanamivir
(Relenza) and
oseltamivir (Tamiflu)
 Adamantanes prevent
viral uncoating in type
Flu season is from November to
march, peaking in February.
Transmitted by aerosols and is
highly contagious. Infection occurs
by binding to epithelial cells of
nasopharynx and regional lymph
nodes and replication occurs in the
respiratory tract.
The infection is self-limiting (2-7
days), starts in URT, replicates and
spreads. Fever chills, headache,
muscle aches, throat pain, cough.
Ciliary columnar epithelium is
destroyed.
Strains identified via hemagglutinin
(viral attachment protein) and
neuraminidase (cell entry via

8.  Influenza A
 Influenza B
 Influenza C
A via M2 protein.
Amantadine &
Rimantadine
ASPRIN + fever/flu =
Reye’s syndrome; Do not
administer asprin.
Vaccines:
 Trivalent inactivated:
contains 2 types of A
and one B; approved for
> 6 month of age.
Contraindicated for
allergies to eggs or
vaccine components,
current illness or
history of Guillian-
Barré syndrome.
 Live attenuated
(LAIV): Better results,
longer immunity and
easier administration
(nasal spray). Can be
given to breast feeding
women.
Contraindicated in > 2
yrs, < 50 years,
immunosuppressed,
pregnant women,
eggs/vaccine
component allergies, on
asprin therapy or
chronically ill.
binding/cleavage of sialic acid).
Negative sense segmented RNA
contained in non-infectious
nucleocapsid.
Can lead to severe lower respiratory
tract infections with desquamation.
Complications: primary viral
pneumonia, secondary bacterial
infections, otitis media, sinusitis, and
croup in infants. Rare complications
include dehydration, myositis,
encephalopathy, Guillian-Barré
syndrome (temp paralysis) and
myocarditis.
Antigenic shift occurs in A only.
Occurs seasonally along with type B.
Has the most antigenic diversity and
can cause pandemics via antigenic
shift.
Type C is normally asymptomatic.
Rubella (German measles)
 RG-I (N America,
Japan, Europe)
 RG-II (Asia)
Paramyxovirus
(Togavirus/
Rubivirus)
NOT an
arbovirus
Diagnostic: isolation of
virus from clinical specimen
valuable for epidemiology,
not diagnosis. Significant
rise in rubella IgG titers, or
the presence of rubella IgM
(parvovirus yields false +)
via ELIZA, IFA or
hemagglutination
inhibition assay.
Prevention: rapidly
deactivated by chemicals,
heat and light. Less
contagious than measles but
most contagious when rash
is erupting.
Vaccine: Live attenuated –
MMR or MMRV; contains
Human reservoir only. Incubation:
14days. One antigenic type with 2
genotypes. Transmitted via
respiratory route, usually late winter
– early spring. Replicates in
nasopharynx and regional lymph
nodes. Produces viremia (5-7 days
after exposure) and is not highly
cytolytic. 50% of cases are
subclinical.
Low grade fever, lymphadenopathy
(occipital, posterior cervical and
postauricular), URT symptoms
precede maculopapular rash (3 days)
beginning on face, spreads to trunk
and limbs,
 Children: rash, hemorrhagic
manifestations, prodrome rare
 Adults: Prodrome (1-5 days)

9.  Progressive
Panencephalitis
 Congenital Rubella
Syndrome
no egg products. One dose
may confer lifelong
immunity. Recommended
for adults born after 1957.
Contraindicated for
pregnant women or those
trying to conceive, acute
illnesses, and
immunocompromised.
May also present with conjunctivitis,
testalgia, orchitis, and soft palate
spots. Arthritis or arthralgia of
fingers/ wrists/knees, encephalitis in
women.
Rare late syndrome of Rubella
Complication that develops in
pregnant women. Can lead to fetal
death or premature delivery, 1st
trimester is most sensitive. Can infect
all organs: deafness, cataracts,
cardiac defects, mental retardation,
bone lesions, hepatitis, or
thrombocytopenia. Delayed
manifestations cause Diabetes
mellitus and progressive
encephalopathy 2-4yrs later.
Teratogenicity possibly due to virus-
induced apoptosis or mitotic arrest of
fetus.
Measles (Rubeola) Paramyxoviridae
(Morbillivirus)
Diagnostic: Koplik’s spots
(white spots/enanthem) on
buccal mucosa before
appearance of rash.
Serological tests for IgM.
Isolation of virus in samples
and detection via PCR.
Giant cells detected in nasal
secretions.
Treatment: Ribavirin used,
but there is no proof that it
is effective. Airborne
precautions.
Vitamin A given in
developing countries to
reduce morbidity due to
pneumonia and diarrhea.
Vaccine: live attenuated
vaccine (MMR) replaced
killed virus vaccine. 2
doses.
Most contagious infectious disease.
Incubation: 11 days. Spread by
respiratory secretions and
multiplies in URT and conjunctiva.
All infections produce clinical
disease.
Produces viremia. One antigenic
type. Recovery imparts lifelong
immunity.
Initial presentation:
 Fever, headache, sore throat
 Koplik’s spots
 The 3 C’s – cough, coryza,
conjunctivitis (with photophobia)
3 days after initial presentation:
 Maculopapular rash starting
on head and working
downward
 Becomes confluent and blotchy
Complications – ear infections, latent
infections, SSPE. Secondary bacterial
pneumonia leading is usual cause of
death. Encephalitis can cause
permanent neurological damage,

10. Atypical Measles
lifelong seizures or psychoses (rare).
Leading cause of death in
malnourished children in developing
countries
Severe vesicular rash, high fever and
edema in extremities upon exposure
to virus after vaccination with
killed vaccine.
Post-infectious (measles)
encephalitis
Diagnostic: history of
measles infection.
Immune-mediated encephalitis after
measles infection.
Subacute Sclerosing
Panencephalitis (SSPE)
Diagnostic: unique lab
abnormalities
Antivirals and interferon
slow progression but
infection will result in death.
Mostly eliminated by
widespread use of MMR
vaccine.
Slowly progressive chronic brain
disorder caused by persistent
measles infection (T2 > T1). Occurs
in children after initial measles
infection with mean incubation
period of 6 yrs.
Highest risk: initial infection in
children under 2 years old
Characterized by inflammatory
lesions in the brain. Presents as mild
changes in personality, slowly
progressing to dementia and death.
Rabies Rhabdoviridae
(Lyssavirus)
(ss enveloped
bullet-shaped
neg-sense RNA)
Diagnostic: evidence of
infection does not occur
until window for
intervention elapses.
Presence of Negri bodies in
neuronal tissue sample, Ag
in CNS/CSF or skin biopsy
at base of neck via IF.
Isolation via cell culture
from CSF or saliva sample.
Ab detected in serum or
CSF.
Treatment: Post-exposure
prophylaxis - Ab can block
spread to CNS if
administered/produced
during incubation period.
Should wash wound with
soap and water, give rabies
serum (half in wound, half
in gluteus muscle), it is
known as HRIG. Start
vaccine series w/ killed
virus on days 0, 3, 7, 14.
Vaccine: preexposure
vaccine (HDCV) for at risk
Zoonotic infection: Transmitted
typically by bite of infected animal.
Primarily by dogs worldwide and
bats (sometimes raccoons) in USA.
Long incubation period where virus
infects muscle and nerve endings.
Varies from 60-365 days. Virtually
always fatal once symptoms develop.
Prodrome phase ensues after
incubation period. Presents with
fever, malaise, headache, pain, or
paresthesias at site of inoculation,
GI symptoms, fatigue, and anorexia.
Prodrome lasts 2-10d then neurologic
symptoms occur.
Neurological symptoms develop via
retrograde axoplasmic transport of
virus to dorsal root ganglia and
spinal cord.
Neuro phase 2-7d. Encephalitis,
neuronal degeneration, hydrophobia,
focal and general seizures, paralysis,
respiratory failure leading to coma.
Patient dies in a few days after coma

11. individuals provides 2 year
protection.
ensues.
Progressive Multifocal
Leukoencephalopathy
(PML)
Polyomavirus -
JC
Diagnostic: PCR assay of
brain biopsy specimen or
CSF
No antiviral treatment
Latent JC virus activates in
immunocompromised/AIDS
(decreased CMI).
Demyelinating disease of brain
white matter that initially causes
visual field defects, mental status
changes, weakness, then rapidly
progresses to blindness, dementia,
coma and death within 6 months.
Prion Disease - Human
 Creutzfeldt-Jakob
Disease
 Variant Creutzfeldt-
Jakob Disease
Hereditary
version can be
mutation in PrP
gene
Autosomal
dominant
mutation in germ
cells
Bovine
Spongiform
Encephalopathy
(BSE) – human
form
Diagnostic: confirmed by
autopsy at death by
characteristic histological
changes in brain tissue
Disease diagnosis made on
clinical grounds based on
symptoms present
No treatment.
Diagnostic: detectible
mutation of PrP gene
Diagnostic: detectible
mutation of PrP gene
identified through genetic
screening
Three kinds:
 Transmissible/Infectious
 Hereditary/genetic
 Sporadic
Disease found mostly in patients over
50 yrs. Presentation similar to
psychiatric disorder
(forgetfulness/disorientation 
dementia), with changes in gait,
involuntary movement, and seizure.
80% with symptoms die in one year.
 iCJD: transmissible via injection
and contact with contaminated
medical devices, transplantation
of contaminated tissues or
cadaveric pituitary growth
hormone
 fCJD: familial/hereditary
genetic
 sCJD: no obvious cause; may be
due to new mutations in somatic
cells. Most common form
 vCJD: Transmitted by ingesting
contaminated beef. Occurs in
much younger patients than CJD.

12.  Gerstmann-Sträussler-
Scheinker (GSS)
Disease
 Fatal Familial Insomnia
(FFI)
 Kuru
Hereditary
mutation
Hereditary
mutation
Transmissible
prion
Cerebellar ataxia and spastic
paraparesis
Progressive insomnia and
dysfunction of autonomic nervous
system leading to dementia and death
Subacute, progressive tremors and
ataxia; does not include dementia
Found in Fore tribe in New Guinea
that practices ritual cannibalism;
transmission likely via skin contact
and not eating contaminated tissue.
Prion disease – animal
 Scrapie
 Bovine Spongiform
Encephalopathy
Transmitted via
consumption of
infected brains
and animal parts
in feed
Diagnostic: has been
transmitted to
mice/hamsters
experimentally for study
Sheep present with tremors, ataxia,
itching that causes them to scrape
their wool off on posts and trees
Endemic in Great Britain; likely
linked to British cases of mad cow
disease cases and occurrence of vCJD
(through consumption of
contaminated beef)
Retrovirus
 Rous Sarcoma Virus
(RSV)
 Mouse Mammary
Tumor virus (MMTV)
 Human Foamy Virus
(HFV)
Retroviridae
(Oncovirinae)
Retroviridae
(Spumavirinae)
Diagnostic: all retroviruses
carry at least 3 genes in
order: 5’-gag-pol-env-3’
 Simple genome has
standard genes + 1 or 2
 Complex genome
contains additional
regulatory and
accessory genes
enabling replication and
virulence
RNA virus particles contain reverse
transcriptase (an RNA-dependent
DNA Pol). Integration is permanent.
Host RNA Pol transcribes proviral
DNA into viral mRNA.
Transducing virus – cell-derived
oncogene from viral genome;
usually replication defective (except
RSV). Also called direct transducing.
Non-transducing virus – cellular
oncogene activated by provirus;
replication competent. Also called
slow transducing.
Human infections have no known
pathology.

13. Human Immunodeficiency
virus (HIV)
 HIV I
 HIV 2
 AIDS
Retroviridae
(Lentiviridae)
Diagnostic: Standard rapid
test is serological ELIZA
assay, which detects Ab to
HIV antigens. If positive,
samples are retested using
Western blot to identify
which Ab is present in
patient serum. PCR detects
proviral DNA (viral load)
and lymphocyte count for
CD4/CD8.
Ab will not be present in
acute phase because virus
replicates rapidly before Ab
can be made.
Treatment: HAART therapy
with at least 3 drugs.
 Reverse transcriptase
inhibitors: nucleoside
analogs (NRTI) stop
DNA synthesis after RT
incorporation and non-
nucleoside reverse
transcriptase
inhibitors (NNRTI)
block the catalytic site.
 Protease inhibitors:
block protein
production through
inhibiting cleavage of
larger proteins.
 Fusion inhibitors:
inhibit gp41 surface
protein from inhibiting
host plasma membrane
 CCR5 antagonists
 Integrase inhibitors
Transmitted by blood, sexual or
parenteral methods. Heterosexual
transmission via vaginal intercourse
and IV drug use are major routes.
Infects CD4+ T-cells and cells of
macrophage lineage via CD4
receptor; coreceptors are CXCR4 (T
cell) and CCR5 (macrophage, T
cell). Can spread via syncytia.
Phasic disease: acute, chronic
(latency) and late phases. Late phase
is clinical manifestation of AIDS.
Most easily spread in acute phase.
Can cause apoptosis of CD4+ T cells.
Causes AIDS.
Primary infection is 2-6wks after
exposure and can be as long as 12-
24wks. Initially presents flu-like
symptoms: fever, chills, night
sweats, malaise, sore throat,
lymphoadenopathy, dry cough and
fever.
Causes less severe form of AIDS
Long latent period, then more rapid
disease progression as immune
system becomes more compromised,
ending in death. Characterized by
opportunistic infections, such as
rashes, thrush, ulcers and rare forms
of cancer and pneumonia.
AIDS Dementia Complex
(ADC)
Also called HIV-1-
associated dementia (HAD)
Incidence decreased by anti-
HIV medications
Pathogenic effects mediated by brain
mononuclear phagocytes, or possibly
by neurotoxic HIV peptides.
Disease caused directly by HIV virus.
Human T-Cell Leukemia
Virus (HTLV)
Retroviridae
(Oncovirinae)
Diagnostic: Presence of
medium to large
multinucleated CD4+ T
cells, flower cells,
indicative for ATLL.
Oncogenic Tax protein
required for ATLL and
TSP/HAM.
Transmitted via blood products,
sexual contact and mother –to-child
(breast-feeding).
Presence of infected cells essential
for transmission.
Virus contains reverse transcriptase
(RNA-dependent DNA Pol); encodes

14.  Adult T cell
leukemia/lymphoma
(ATLL)
 HTLV-I-associated
myelopathy/tropical
spastic paraparesis
 Infective dermatitis
Immunophenotypic
assessment: characteristic
presence (CD2, CD3, CD5)
or absence (TdT, CD1a) of
cell markers or activation of
lymphocytic markers (HLA-
DP, DQ, DR and IL2-alpha
R).
Serology for HTLV-1 Ab.
All assays are confirmed
with PCR for monoclonal
integrated provirus.
Treatment: None effective
for ATLL or TSP/HAM.
Median survival with
treatments less than 1 year.
tax and rex genes critical for
initiation of oncogenesis.
Infects CD4+ T cells; viral entry
requires presence of heparin sulfate
proteoglycans (HSPG), Neuropilin
1 (NRP-1) receptor and GLUT1
receptor. Only 5% of carriers develop
disease with HTL-1. HTL-2 not
associated with disease.
ATLL develops 10-30 years after
initial infection. Causes
immunocompromised condition and
opportunistic infections. 4 subtypes:
 Acute: 57%, presents with
fever, cough, lymphoadenopathy,
skin and lung lesions,
leukocytosis, hypercalcemia 
lytic bone lesions and bone
resorption. Avg survival- 6
months.
 Lymphoma: presents with
lymphoadenopathy,
skin/cutaneous lesions, impaired
hepatic function and
hypercalcemia. Avg survival-
10 months.
 Chronic: 19%, presents similar
to but with much milder
symptoms than acute type.
Fewer leukemia cells in
peripheral blood. Avg survival-
24 months.
 Smoldering: 5%, presents with
skin and lung lesions. Low level
of leukemia cells in peripheral
blood. Avg survival- long
duration.
Presents like multiple sclerosis, with
degeneration of myelin in the CNS.
Occurs frequently in Jamaica.
Presents as crusty skin lesions; co-
infection with staphylococcus aureus
and beta-hemolytic streptococcus.

15. DNA Tumor Viruses
 EBV
 KSHV
 SV40
 HPV
 BK, JC viruses
Adenoviridae
Poxviridae
Herpesviridae
Herpesviridae
Papovaviridae
(polyomavirus)
Papovaviridae
(Papillomavirus)
Papovaviridae
(polyomavirus)
Diagnostic: Cells have
altered morphology; appear
rounded (disaggregation of
actin) and more refractile.
DNA tumor viruses encode an
oncoprotein. In most cases, they
transform only cells in which they
cannot replicate (non-permissive).
B cell proliferation. Can cause
Hodgkin’s lymphoma, Burkitt’s
lymphoma and nasopharyngeal
carcinoma.
 LMP1 targets TRAFs
Causes Kaposi’s sarcoma (KS),
primary effusion lymphoma (PEL),
Castleman disease (MCD).
Replicates in African green monkey
(origin) where it causes cytopathic
effects but no tumors. No replication
in rodent cells - causes malignant
transformation. Experimental model.
 Large T Ag targets p53 and
pRb
 Small T Ag targets PP2A
Both large T antigen and small T
antigen is necessary for viral DNA
replication in permissive cells. One
of the T antigens required to be
produced at all times to keep the cell
transformed.
Causes anogenital warts and
carcinomas, cervical cancer,
oropharyngeal carcinomas
 E6 targets p53, DLG, MAGI-1,
MUPP1
 E7 targets pRb
Merkel cell tumor associated with
polyomavirus.
Herpes Simplex Virus
(HSV)
Type 1 & Type 2
Herpesviridae
(Human
Herpesvirus)
Diagnostic: Tzanck smear,
Wright’s/Giemsa for giant
cells, immunofluorescence,
can culture
Antivirals:
Acyclovir, Famciclovir,
Valacyclovir
“Umbilicated vesicles”
Type 1:
 Fever blisters/Cold sores
 Ophthalmic  blindness
 Eczema herpeticum (widespread
atopic dermatitis)
 Chronic herpes ulcers
(immunodeficiency, AIDS)

16. Type 2:
 Genital Herpes
 Neonatal disseminated HSV
(acq. at birth)  fatal if
untreated
 Congenital disseminated HSV
(acq. in utero)  usually fatal
Chicken Pox (varicella)
Shingles (zoster)
Herpesviridae
(Human
Herpesvirus)
Diagnostic: Tzanck smear,
immunofluorescence, not
culture sensitive
Antivirals:
High dose Acyclovir,
Famciclovir, Valacyclovir
Vaccines available for both
Red macule  papule  vesicle
(dew drop on rose petal)  pustule
 crusted ulcer
Rash in one dermatome, usually one
episode
 Disseminated zoster  fatal if
untreated (immunodeficiency,
AIDS)
 Ophthalmic  blindness
Warts Papillomavirus
(various)
Many treatments available,
none work great
 Topical salicylic acid
 Liquid nitrogen
 Laser removal
 Imiquimod
Condyloma acuminatum Papillomavirus
(various)
Difficult to treat
 Podophyllin
 Podophyllotoxin
 Sinecatechins
 Cryosurgery
 Imiquimod
 Laser
 Interferon
Quadrivalent vaccine
(6, 11, 16, 18)
Venereal warts
Some viral types associated with
increased risk of cancer
 Cervical
 Vulvar
 Anorectal
Molluscum contagiosum Poxvirus Diagnostic: Biopsy shows
large viral inclusion bodies
Self-resolves in 6-12 months
without treatment
 Curettage
 Cryosurgery
 Imiquimod
 Wart treatments
“Umbilicated papules”
Cryptococcus may mimic in AIDS,
immunosuppressed

17. Smallpox
Milker’s nodule
Orf (ecthyma contagiosum)
Poxvirus Vaccine limited smallpox
infections but is no longer
administered.
Milker’s nodule and Orf are
self-limiting.
Bioterrorism concern
Erytematous papules evolving at
same rate, become pustular , esp. face
and extremities
Papules, often on hands, common in
farmers handling livestock (cattle,
sheep, goats)
Kaposi’s sarcoma Herpesvirus 8 Vascular tumor often seen in patients
with AIDS
Pityriasis rosea Unknown –
currently thought
to be viral
Initial herald patch is “ringworm-
like”, then oval scaly lesions form on
trunk and proximal extremities
Exanthems:
 Measles
 Scarlet fever
 German measles
 Duke’s disease
 Erythema infectiosum
 Roseola/ exanthem
subitum
Streptococcus
(non-viral)
Parvovirus B19
Human
Herpesvirus 6
Treatment: penicillin
Rashes
See Measles
“Sandpaper-like” erythematosus
non-pruritic rash, “strawberry”
tongue
See Rubella
Described, no longer present
“Slapped cheek fever”
 Bright red rash on cheeks
followed by evanescent
reticulated rash on extremities,
face, neck and trunk.
 Arthritis/lupus-like symptoms
possible in adult females,
premature labor and birth
anomalies
 Aplastic crises in sickle cell or
anemic patients
High fever and erythematosus
macular rash that begins when fever
suddenly drops (can be mistaken for
reaction to antibiotic); usually in
infants

18.  Others  Coxsackie (hand, foot and mouth
disease)
 Non-specific rash with
echoviruses
 Infectious mononucleosis (EBV)
produces palatal petechiae;
severe rash develops if treated
with ampicillin or amoxicillin
 Dengue fever (Flavivirus)
produces scarlet fever-like rash
and/or severe (often fatal)
hemorrhagic eruptions
Gold/Orange – Rash
Blue – Respiratory
Red – Slow viruses (involve CNS)
Green – generalized and GI
Brown - Tumor viruses
Purple – Retroviruses
Liver Panel Values:
AST (aspartate transaminase) 8 – 40 IU/L
ALT (alanine transaminase) 30 – 65 IU/L
GGT (gamma glutamyl transpeptidase) 5 – 85 IU/L
Bilirubin 0.1 – 1.1 mg/dL