The Reoviridae Family: by Luka, Mela Ilu
The Reoviridae Family: by Luka, Mela Ilu
The Reoviridae Family: by Luka, Mela Ilu
By
Luka, Mela Ilu (UJ/2014/PGMD/0104)
Department Of Medical Microbiology
Faculty Of Medical Sciences
University Of Jos
INTRODUCTION
The development of Reoviridae as a
family in its own right has been
fairly recent.
This happened when Albert Sabin
suggested that the viruses which
had until then been classified as
belonging to the echovirus 10
group be set apart as a brand new
family- this was in 1959.
INTRODUCTION...
The acronym REO (Respiratory
Enteric Orphan) was suggested to
denote that these agents were isolated
from the respiratory and enteric tracts
and had not been associated with any
disease (orphan virus).
The first human Orthoreovirus was
isolated in 1953 from a rectal swab
collected from a healthy child and was
originally the prototype for echovirus
type 10 of the Picornaviridae family.
CLASSIFICATION
The Reoviridae contains 15 genera which
are divided into two subfamilies;
Spinareovirinae and Sedoreovirinae
based on the presence of a spike or
"turret" protein on the inner capsid.
The genera of Spinareovirinae subfamily
are; Aquareovirus, Coltivirus, Cyptovirus,
Figivirus, Orthoreovirus, Idnoreovirus,
Dinovernavirus, Oryzavirus, Mycoreovirus
The genera of Sedoreovirinae are;
Cardoreovirus, Mimoreovirus, Orbivirus,
Phytoreovirus, Rotavirus, Seadornavirus
CLASSIFICATION
Phylogenetic comparison of the viral
polymerase protein sequences of viruses
of the family Reoviridae indicates a
common phylogenetic origin between
seadornaviruses and rotaviruses.
Out of these 15 genera, only four are able
to infect humans and animals; these are
Orthoreovirus, Rotavirus, Coltivirus and
Orbivirus. Four genera infect only plants
and insects and one infects fish.
The virus of clinical concern in this family
is the rotavirus.
OTHER REOVIRIDAE
Aquareovirus
2.
Rotavirus
3.
Seadornavirus
4.
Coltivirus
5.
Fijivirus
6.
Phytorireovirus
7.
Mimoreovirus
Algae
8.
Orbivirus
9.
Cypovirus
10.
Orthoreovirus
Vertebrates
11.
Idnoreovirus
Hymenoptera
12.
Dinovernavirus
Insects, mosquitoes
13.
Oryza virus
14.
Cardoreovirus
Crustaceans: crabs
15.
Mycoreovirus
Fungi
Rotaviru
s
Discovered by Ruth Bishop
and her colleagues by
electron microgram image
in 1973
VIRAL CLASSIFICATION
INTRODUCTION
Rotavirus is the most common cause
of severe diarrhoea and vomiting
among infants.
Nearly every child in the world has
been infected with rotavirus at least
once a year by the age of five.
There are 8 species of this virus
referred to as A, B, C, D, E, F, G and H.
Rotavirus A is the most common
species and causes more than 90% of
rotavirus infection in humans.
GENOMIC STRUCTURE
They are non-envelope, 60-80 nm in diameter, possess 2
concentric capsid shells, each of which is icosahedral.
The genome consists of double-stranded RNA in 10-12
discrete segments, with a total genome size of 16-27
(kbp).
The individual RNA segments vary in size from 680 to
3900 bp. The virion core contains several enzymes
needed for transcription and capping of viral RNA.
The core is composed of 3 major (i.e., lambda-1, lambda2, sigma-2) and several minor proteins that surround 10
segments of double-stranded RNA.
Reoviruses are unusually stable to heat, stable to wide
range of pH (3.0-9.0), and to lipid solvents, but they are
inactivated by 95% ethanol, phenol, and chlorine.
STRUCTURE OF ROTAVIRUS
REPLICATION
EPIDEMIOLOGY
Rotaviruses are the single most important
worldwide cause of gastroenteritis in young
children.
Typically, up to 50% of cases of acute
gastroenteritis of hospitalized children
throughout the world are caused by
rotaviruses.
In temperate climates, rotaviruses are
responsible for a large number of cases of
diarrheal disease in the winter. The
seasonality of rotavirus disease is less
apparent in tropical climates but is still more
prevalent in the drier than cooler months.
EPIDEMIOLOGY
Rotavirus is estimated to cause
about 50% of all hospital
admissions due to diarrhoea among
children > 5yrs world wide.
This leads to 100 millions episodes
of acute diarrhoea each year that
results in 350,000 to 600,000 child
deaths. (WHO)
TRANSMISSION
Transmission appears to be by faecal-oral
route, with little evidence of airborne
transmission.
Adult contacts may be infected, as
evidenced by seroconversion, resulting from
contact with children that are infected.
However, epidemics of severe disease have
occurred in adults, especially in closed
populations, as in a paediatric ward.
Nosocomial infection is also frequent.
The presence of rotavirus in the faeces is
not always associated with symptomatic
disease
PATHOGENESIS
Infection is initiated in the upper
intestine and typically leads to a
series of histologic and physiologic
changes. The incubation period is
brief.
Rotavirus replicates in the mucosal
cells of the small intestine,
resulting in the excess secretion of
fluids and electrolytes into the
bowel lumen.
One of the rotavirus-encoded
PATHOGENESIS
Damaged cells may slough into the lumen of
the intestine and release large quantities of
viruses, which appear in stool (up to 10 12
particle per gram of faeces).
Diarrhoea caused by rotaviruses may be due
to impaired sodium and glucose absorption
as damaged cells on villi are replaced by no
absorbing immature crypt cells.
3 to 8 weeks may be necessary for normal
function to be restored. Antibodies present
in the intestinal lumen have been shown to
play a role in the passive protection of
young animals.
IMMUNITY
Immunity to rotavirus infection is
unclear.
It is likely that intestinal IgA
directed against specific serotypes
protects against reinfection and
that colostrum IgA protects newborns up to the age of 6 months.
By age 3 years, 90% of children
have serum antibodies to one or
more types.
IMMUNITY
Asymptomatic infections are more
common with successive
reinfections.
Local immune factors, such as
secretory immunoglobulin A (IgA)
or interferon, may be important in
protection against rotavirus
infections.
Asymptomatic infections are
common in infant before age 6
months.
CLINICAL MANIFESTATIONS
Rotaviruses induce a clinical illness
characterized by vomiting,
diarrhoea, abdominal discomfort,
fever, and dehydration.
The duration of hospitalization
ranges from 2 to 14 days with a
mean of 4 days.
The highest rate of attack is in
young children between 6 to 12
months, then those less than 6
months.
CLINICAL MANIFESTATION
Rotaviruses also induce chronic
symptomatic diarrhoea in
immunodeficient children, with an
occasional fatal outcome.
Rotavirus infections can especially
be severe and sometimes fatal in
individuals of any age who are
immunosuppressed for bone
marrow transplantation.
Rotavirus infections have also been
associated with necrotizing
DIAGNOSIS
Lab. diagnosis
requires
identifying the
virus in faeces or
rectal swab
specimens.
Demonstrating a
4-fold or greater
increase in
antibody to a
rotavirus antigen
between acuteand convalescent-
DIAGNOSIS
Other methods include;
Electron microscopy
Radioimmunoassay
Counter immunoelectro-osmophoresis
Immunofluorescence
Inoculation of tissue cultures
Latex agglutination
Reverse passive hemagglutination assay
Polyacrylamide gel electrophoresis
Dot hybridization, PCR, and ELISA.
TREATMENT
There are no viral-specific or antiviral
drugs for treatment of rotavirus
infection.
The primary aim of treatment of
rotavirus gastroenteritis is replacement
by the intravenous or oral route of
fluids and lost by vomiting or
diarrhoea.
Human milk that contains rotavirus
antibody is effective when given orally
to treat immunodeficient patients with
chronic rotavirus infection.
TREATMENT
Human immune serum globulin (globulin) that contains rotavirus
antibody was given prophylactically
(orally) to low birth-weight infants
in a nursery in which recurrent
rotavirus infections occurred.
The solution recommended by WHO
contains 30 mEq/L of sodium, 30
mEq/L of potassium, and 30 mEq/L
of bicarbonate.
PREVENTION/CONTROL
The best method of preventing
rotavirus infection is vaccination.
Two rotavirus vaccines are
available; these are Rotatix and
Rotateq. Both contain live virus and
are given orally.
Careful attention to hand washing,
disinfection, proper sewage
disposal, wastewater treatment,
good sanitation and disposal of
contaminated material may limit its
Coltivirus
Types species: Colorado tick
fever virus
VIRAL CLASSIFICATION
VIROLOGY
They are about 60 90nm in
diameter
Non enveloped
Spherical in shape with icosahedral
symmetry
Possess 2 concentric capsid shells
surrounding a core of about
50nmin diameter
Inactivated at pH of 3 but stable at
7 and 8
Stop being a threat at a
EPIDEMIOLOGY
The distribution of colorado tick
fever virus is in the rocky
mountains of area of the US at
elevations between 4 and 10
thousand feet.
Found in places like California,
Colorado, Idaho, Montana, Nevada,
Utah, Columbia etc
The virus circulates between ticks
and rodents, with humans being
the secondary hosts (Kapikian,
PATHOGENESIS
The virus replicates in bone marrow
cells which disrupts the
development and replication of
leucocytes, eosinophils and
basophils
They stay within the RBC without
harming it up to 4 months being
protected from the immune
systems attacks.
Antibody to the virus is found only
about 2 weeks after the symptoms
SYMPTOMS
Fever
Rash
Chills
Headache
Photophobia
Myalgia
Arthralgia
Lethargy
Haemorrhagic disease
Leukopaenia with
both lymphocytes and
neutrophils is
common
SYMPTOMS
DIAGNOSIS
Reverse
Transcriptase
Polymerase
Chain Reaction
(RT-PCR)
Immunoflouresce
nce microscopy
TREATMENT
No known vaccine treatment
3- fluors-3- deoxyadenosine, a
nucleoside analog, halt replication
of colorado tick fever virus in vitro
CONTROL
Wearing long sleeves or
pants
Avoiding high tick infested
areas
Use of tick repellant
Seadornavirus
Type species:
Banna virus
VIRAL CLASSIFICATION
INTRODUCTION
Two other species in this genus
are; Kadipiro virus and Liao ning
virus. Each of these viruses has
been isolated in Aedes, Anopheles
and Culex. Only Banna is known to
cause disease in humans.
Human, cattle, pig and mosquitoes
serve as the natural host.
The word Seadornavirus is an
acronym, meaning Southerneast
Asian dodeca RNA virus
STRUCTURE
Non-envelope
Icosahedral geometry
The diameter is around 60 70nm
Genomes are linear and segmented
Segment range in length from 862
to 3747 base pairs
The genomes code for 12 proteins
REPLICATION
Viral replication is cytoplasmic.
Entry is by attachment to the host
receptors which mediate
endocytosis
Replication follows the dsRNA virus
replication model. dsRNA virus
transcription is the method of
transcription.
The virus exits the host cell by
monopartite non-tubule guided
viral movement.
EPIDEMIOLOGY
These viruses are endemic in
Southeast Asia, particularly India
and China.
Banna virus was first isolated in
1987 from CSF and sera of patients
with encephalitis in South and
western China in patients with
fever and flu-like manifestation.
SUMMARY
Symptoms; encephalitis, malaise and
fever
Diagnosis; ELISA, 4 fold increase in
IgG antibody, and PCR
Treatment; no vaccine available,
treatment is symptomatic
Control; measures that prevent
mosquito bite of humans
REFERENCES
Bernstein DI, Glass RI, Rodgers G. et al. Evaluation of rhesus
rotavirus monovalent and tetravalent
reassortmen/vaccines in U.S.
Children.JAMA.1995;273:1191.
Carlson JAK, Middleton PJ, Szymanski M. et al. Fatal rotavirus
gastroenteritis Analysis of 21 cases.Am J Dis
Child.1978;132:477.
Cook SM, Glass RI, LeBaron CW, Ho M-S. Golbal seasonality of
rotavirus infections.Bull WHO.1990;68:171.
Davidson GP, Whyte PBD, Daniels E. et al. Passive
immunization of children with bovine colostrum
containing antibodies to human
rotavirus.Lancet.1989;2:709.
REFERENCES
Emmons RW. Ecology of Colorado tick fever.Annu Rev
Microbiol.1988;42:49.
Guarino A, Canini RB, Russo S. et al. Oral
immunoglobulins for treatment of acute rotaviral
gastroenteritis.Pediatrics.1994;93:12.
Hoshino Y, Kapikian AZ. Rotavirus vaccine development
for the prevention of severe diarrhea in infants and
young children.Trends in Microbiol.1994;2:242249.
Kapikian AZ, Chanock RM: Rotaviruses. p. 1353. In Fields
BN, Knipe DM (eds): Virology. Vol.2. Plenum, New
York, 1990 .
Thank
You