ORTHOMYXOVIRIDAE  causes inflammation of the upper respiratory

tract from 1-6 years of age

 Wilson Smith, C.H. Andrewes, P.P. Laidlaw at London
 diagnosis: RT-PCR targeting the viral M or NP
National’s Institute for Medical Research (1933)
genes, virus isolation in tissue culture
 80-120 nm
 control: no vaccines
 enveloped with helical capsid that encloses a single-
stranded negative sense RNA genome REOVIRIDAE
1. influenza A
 famous poliovirus vaccine researcher, Albert B. Sabin
 segmented (eight separate molecules),
(1959)
single-stranded, RNA genome
 first named respiratory-enteric-orphan virus
 helical capsid with envelope
(reovirus)
 viral subtypes based on hemagglutinin and
 60-80 nm
neuraminidase glycoproteins abbreviated “H”
 genome: linear, double-stranded, segmented RNA
and “N”
(10-12 segments) with individual RNA segments
 infects humans and other animals
ranging from 680-3,900 bp, totaling 16-27 kbp
 antigenic drift, causes local outbreaks of
1. rotavirus
influenza every 1-3 years
 “rota”, meaning wheel
 MOT: Contact with respiratory secretions
 70 nm
 headache, chills, fever, malaise, myalgias,
 wheel-shaped particle, with double-layered
anorexia, and sore throat
icosahedral capsid
 fever rapidly climbs to 101 to 104°F (38.3 to
 RNA segments 1, 2, 3, and 6 — inner capsid
40.0°C)
polypeptides (VP1, VP2, VP3, and VP6,
 diagnosis: RT-PCR
respectively)
 control: influenza vaccine or antiviral
 RNA segments 4 and 7, 8, or 9 — outer capsid
prophylaxis
polypeptides (VP4 and VP7, respectively)
 treatment: supportive; antivirals
 Family Reoviridae
amantadine and rimantidine (influenza A
 MOT: fecal-oral route, possibly respiratory
only), and zanamivir and oseltamivir
route
influenza A and B
 infects infants and young children (30-50% of
2. influenza B
cases worldwide)
 similar to “mild” influenza
 temperate climates: peaks in winter
 cause seasonal epidemics (known as flu
 tropics: occurs year round
season)
 hospitalization: 2-14 days
 enveloped virus, eight single-stranded RNA
 normal neonates: no clinical manifestations.
molecules
 neonates in SCU: necrotizing enterocolitis
 antigenic drift only, resulting in local
and hemorrhagic gastroenteritis
outbreaks every 1-3 years
 immunodeficient children: chronic
 MOT: Contact with respiratory secretion
symptomatic diarrhea
 incubation period: 1-3 days
 immunosuppressed individuals: severe and
 diagnosis: Cell culture (PMK), EIS, FA stain,
sometimes fatal
RT-PC
 incubation period: < 48 hrs.
 control: influenza vaccine or antiviral
 diagnosis: examination of specimen by
prophylaxis
negative-strain electron microscopy
 treatment: antivirals zanamivir and
 control: fluids and electrolytes replacement
oseltamivir
(for dehydration), careful attention to
3. influenza C
handwashing, disinfection, and disposal of
 humans are the main reservoir but the virus
contaminated material, especially in
may also infect dogs and pigs
nurseries and hospitals where nosocomial
 morphologies: elliptical, spherical, or
infections occur frequently
filamentous
 80–120 nm
RETROVIRIDAE  Anti-HIV Igm (appears after one week of
onset of HIV infection)
 “retro” = backward
 Anti-HIV IgG (appears 3-6 weeks after
 by Peyton Rous
infection)
 Avian virus
 Control: Blood screening tests for HIV
 Rous Sarcoma Virus (1911)
infection, Antiretroviral Therapy,
 80–110 nm
ABSTINENCE
 Helical nucleoprotein within icosahedral capsid 3. Human immunodefieciency virus 2
 Composition: RNA (2%), protein (about 60%), lipid  plasma viral load: 10,000 copies/mL
(about 35%), carbohydrate (about 3%)
 genome: 9,800 nucleotides
 Genome: Single-stranded RNA, linear, positive-
 groups: A-H
sense, 7–11 kb, diploid
 capsid: p26
 Proteins: Reverse transcriptase enzyme contained
 site of latent infection: CD4 T cells
inside virions
 MOT: Sexual contact, Blood transfusion and
 Replication: Reverse transcriptase makes DNA copy
Organ transplant, Sharing of injections,
from genomic RN
Mother-to-child transmission
 Maturation: Virions bud from plasma membrane
 Primary stage: Acute HIV infection
Gammaretrovirus Murine leukemia virus  Intermediate stage: clinical latency / chronic
Epsilonretrovirus Walleye dermal infection
sarcoma virus  Final stage: AIDS (slow progression)
Betaretrovirus Mouse mammary  Diagnosis: Rapid Tests, ELISA (Screening
tumor virus test), Western Blot (Confirmatory Test)
Alpharetrovirus Avian leukosis virus  Anti-HIV Igm (appears after one week of
Lentivirus Human onset of HIV infection)
immunodeficiency  Anti-HIV IgG (appears 3-6 weeks after
virus 1
infection)
Delataretrovirus Human t lymphocytic
 Control: Blood screening tests for HIV
virus
infection, Antiretroviral Therapy,
Spumavirus Simian foamy virus
ABSTINENCE

1. Human immunodeficiency virus 4. Human t lymphocytic virus 1& 2

 Genus lentivirus
 Proteins: gp41/gp120 complex, p24, p17
2. Human immunodeficiency virus 1
 Plasma viral load: millions of copies/mL
 Genome: 9,200 to 9,600 nucleotides
 Groups: m, n, o
 capsid: spherical, cylindrical, or conical,
Fullerene cone model
 site of latent infection: CD4 T cells
 MOT: sexual contact, blood transfusion,
organ transplant, sharing of injections,
mother to child
 Primary stage: Acute HIV infection
 Intermediate stage: clinical latency / chronic
infection
 Final stage: AIDS (fast progression)
 Diagnosis: Rapid Tests, ELISA (Screening
test), Western Blot (Confirmatory Test)
 Enveloped, single-stranded RNA virus
 Virion: spherical
 Capsid: icosahedral
 Genome: 9k bases in length, encodes
accessory and regulatory genes
 HTLV 1 (1979): first isolated from human T-
cell line, DISEASE: Adult T-cell leukemia
(1977) - infectious etiology
 HTLV 2: second isolated, DISEASE: Hairy cell
leukemia
 Both are closely related, with some
serological cross reactivity between the two.
 80-100 nm
 Genus: oncovirinae
 Incubation period: 1-2 months
 Site of latency: t lymphocytes
 At risk groups: children born to infected
mothers, sexual partners of infected
 individuals ,who receive infected blood
products , IV drug users
 HTLV 1 clinical illnesses : ADULT T-CELL
LEUKEMIA OR LYMPHOMA (ATL)
 - takes 30-50 years to develop after HTLV
1 infection &
 HTLV associated myelopathy (HAM) or
Tropical spastic paraparesis
 - more common in adults and females,
 MOT: sexual route,
 Latent period: months to years
 HTLV 2 clinical illnesses: HAIRY CELL
LEUKEMIA - B cell neoplasm and involves
peripheral blood, bone marrow, spleen and
liver
 -affects middle-aged to elderly men
 -male to female ratio of 5:1
 Diagnosis: Serology Enzyme-linked
immunosorbent assays (EIAs), Western
blot tests, HAM/TSP: serum HTLV
antibody can be demonstrated in the
CSF, PCR (HTLV 1), ELISA KIT HTLV 1 and
2
 Control: Reducing vertical transmission,
Screening of all blood or organ donors,
Safe sex, Avoidance of sharing drug
injecting equipment