Virology: Poison
Virology: Poison
chemicals
Enveloped viruses
INTRODUCTION
– have bilayered envelope
Family: viridae
– more fragile and pleomorphic
Beijerinck (1897) – Latin name “virus” : – envelope may come from the host
poison cell membrane
intracellular
ultimate parasite Viral Replication
do not grow larger and divide like any STEPS
other organism 1. Adsorption/Attachment
- to initiate the infectious cycle, a virus
General Characteristics must first recognize and bind to a suitable
Nonliving structures host cell.
Contain a protein coat called the capsid
Have a nucleic acid core containing DNA 2. Penetration
or RNA (one or the other-not both) - Direct penetration of cell membrane
Not susceptible to antibiotic (Naked)
Capable of reproducing only when inside - Fusion with cell membrane (Enveloped)
a HOST cell - Receptor-mediated endocytosis
To diagnose: C. Molluscipoxvirus
Papanicolau staining (koilocytosis) - causes molluscum contagiosum
*Koilocytes- vacuolated or inclusion
bearing cells ADENOVIRUSES
- Naked, icosahedral viruses with linear, ds
B. Polyomaviruses DNA
1. BK Virus - Orbiting satellite
- obtained from urine of patient receiving - 10 structural proteins (2 most important
immunosuppressive therapy after kidney are the hexons and pentons)
transplant - Hexons- reactive antigen
2. JC virus
- obtained from brain of patient with Causes:
PML (Progressive Multifocal • Localized respiratory outbreaks – Types
Leukoencephalopathy) 1 to 7 & 21
• Swimming pool associated
*PML-a rare disease involving plaques of pharyngoconjunctivitis – Types 1-7
demyelization/inflammation of the CNS seen in • Epidemic keratoconjunctivitis – Type 8
elderly and immunocompromised hosts • Adenovirus type 12 – most studied;
caused tumors to rodents
Portal of entry for JC and BK viruses is the • Gastroenteritis – types 40 & 41
urinary tract • Acute hemorrhagic cystitis –types 11 &
12
• Cervical lesions/urethritis (males)
Lentiviruses
Diagnosis: A. HIV-1 - from the Latin term lentus
* CPE :swollen cells in grape-like clusters meaning slow (lengthy/insiduous onset)
- Acquired Immunodeficiency Syndrome
PARVOVIRUS
Parvovirus (B19) Replication
- small, naked, icosahedral virus with • Binds specifically to CD4 receptor (T-
ssDNA helper cells)
- kite-shaped wedge nucleocapsid • Penetrates cell by fusion
- tropic for human erythroid cells • Released by budding from plasma
- It causes transient aplastic crisis, a self- membrane
limited erythropoeitic arrest. The gp120 protein on virus binds
- Latin: parvus (small) specifically to CD4 receptor on host
- Replicates in adult’s bone marrow and cell with high affinity.
fetal liver Gp41 causes fusion of the virus to the
Causes: cell membrane.
1. Erythema infectiosum - “Slapped After fusion, virus particle enters
cheek syndrome” or 5th disease cell.
2. Transient aplastic anemia Viral genome exposed by uncoating
3. Pure red cell aplasia particle.
4. Hydrops fetalis - fatal anemia of
babies, no physical abnormalities Stages:
1. Primary HIV Syndrome
Medically Important RNA Viruses - Mononucleosis-like, cold or flu-like
symptoms may occur 6 to 12 weeks after
RETROVIRUSES (transcribe RNA to DNA) infection.
- Spherical with a tree-like layered Lymphadenopathy, fever, rash,
structure, in the center are two identical headache, fatigue, diarrhea, sore
copies of the ss RNA associated with throat, neurologic manifestations ,no
reverse transcriptase and surrounded symptoms may be present
by an icosahedral capsid Symptoms are relatively nonspecific.
- Outer envelope contains a lipid matrix HIV antibody test often negative but
within which specific viral glycoproteins becomes positive within 3 to 6
are embedded. months, this process is known as
These knob-like structures responsible seroconversion.
for binding to target cell. Large amount of HIV in the
peripheral blood.
Former names of the virus include: Primary HIV can be diagnosed using
- Human T cell lymphotrophic virus viral load titer assay or other tests.
(HTLV-III) Primary HIV syndrome resolves
- Lymphadenopathy associated virus itself and HIV infected person
(LAV) remains asymptomatic for a
- AIDS associated retrovirus (ARV) prolonged period of time, often
years.
Discovered independently by Luc Montagnier
of France and Robert Gallo of the US in 1983-
84.
2. Clinical Latency Period o gp120 and gp41 both involved
- Infected individuals are at risk for with fusion and attachment of
opportunistic infections (CD4 count HIV to CD4 antigen on host cells
<500) gag- group-specific antigens (encodes
HIV continues to reproduce, CD4 count the viral core) located in the nucleocapsid
gradually declines from its normal value of the virus (p24)
of 500-1200. o p24 is the core antigen
Pol- polymerase (encodes the reverse
Diseases Predictive of AIDS progression: transcriptase enzyme)
1. persistent herpes-zoster infection (shingles) - Responsible for conversion of viral RNA
2. oral candidiasis (thrush) into DNA
3. oral hairy leukoplakia
4. Kaposi’s sarcoma (KS) Transmission: blood transfusion, sexual
intercourse, intravenous drugs, perianal infection
3. Full-blown AIDS
- 10-11 years from primary to full-blown Major Risk Groups :
AIDS - promiscuous homosexuals and bisexual
- CD4 count <200 men
Pneumocystis carinii pneumonia - prostitutes
(PCP) - intravenous drug users
Cryptococcal meningitis - blood recipients
Toxoplasmosis - hemophiliacs
- If CD4 count <50 - sexual contacts of these groups
Mycobacterium avium - newborn children born to infected mothers
CMV infections
Lymphoma Sustiva + Truvada is one of the most popular and
Dementia effective starting HIV regimens.
Most deaths occur with CD4 Truvada is made up of HIV drugs from a
counts below 50. class called nucleoside/nucleotide
reverse transcriptase inhibitors (NRTIs),
Diagnostically Important HIV Antigens : also known as “nukes.”
a. p24 The NRTIs block reverse transcriptase, a
b. gp41 protein that HIV needs to make more
c. gp120 copies of itself. This may slow down HIV
d. gp160 disease