PARVOVIRUS

(B19)
HANNAH PATRICIA P. LANASA
HANNAH PATRICIAM33
P. LANASA
M33
 What is a
Parvovirus
(B19) ?
Parvoviruses are non-enveloped, icosahedral
particles 18 to 26 nm in diameter. Plus and minus
DNA strands are packaged into separate virions
in approximately equal proportion. There are two
capsid proteins
• The name B19 was coined after the sample
number containing the virus; panel B and
no.19, during the screening of hepatitis B virus
• B19V infection causes several diseases in
humans, including like fifth disease in
children, Transient aplastic crisis, non-
immune hydrops fetalis in pregnant women
PARVOVIRUS B19 Infects only humans !

Human Parvovirus only get infected by coming

into contact with a dog or cat parvovirus. A cat
or dog cannot also contract parvovirus B19 from
an infected person

Other parvoviruses that do not infect humans

can infect pets such as dogs and cats. You can
protect your pets from parvoviruses by
vaccinating them.
 FIFTH DISEASE
ERYTHEMA
INFECTIOSUM
• viral disease that often
results in a red rash on the
arms, legs, and cheeks.

• “slapped cheek disease.”

• It's fairly common and mild

in most children.

• more severe for pregnant

women or anyone with a
 TRANSMISSION
ANIMALS
Since parvovirus B19 only
infects humans, a person cannot get the
virus from a dog or cat.
Also, dogs and cats cannot get parvovirus
B19 from an infected person.
Pet dogs and cats can get infected with
other parvoviruses that do not
infect humans.
HUMANS
• It spreads through respiratory
secretions, such as saliva,
sputum, or nasal mucus, when
an infected person coughs or
sneezes.
•  Parvovirus B19 can also spread
through blood or blood
products.
 MOST COMMON SYMPTOMS

FEVER RUNNY NOSE HEADACHE

These symptoms pass, and the illness seems to be
gone until the rash appears a few days later. Kids
younger than 10 are most likely to get the rash. The
bright red rash usually starts on the face. Then, red
blotches (usually lighter in color) appear on the trunk,
arms, and legs. After a few days, the rash, which can
be itchy, takes on a lacy net-like look.
 PREVENTION

DISINFECTION
COVER DISTANCE Use aerosol sprays,
Cover the mouth and Avoid contact to alcohols etc to
nose when coughing anyone who is sick prevent the viruses in
or sneezing contact with your
child

BE CLEAN HANDWASHING STAY HOME

Do not touch the
Wash hands with Keep them home
eyes, nose and
soap and water when they are sick
mouth without
washing
 TABLE OF CONTENTS

01. VIRAL STRUCTURE 02. SURFACE ANTIGENS

03. VIRAL PROTEINS 04. CORRELATIONS

 01.
VIRAL STRUCTURE
Human B19 virus is a nonenveloped, icosahedral virus
with a diameter of 18 to 26 nm. The virus capsid is
composed of two structural proteins. Structural
proteins VP-l and VP-2 have molecular weights of
83,000 and 58,000, respectively, and account for 60 to
80 percent of the virion mass. The DNA genome is 5.5
kilobases long and the virus packages plus and minus
DNA strands into separate virions with equal
efficiency. It is very hardy and viral infectivity is
resistant to ether, chloroform, deoxyribonuclease
(DNase) and ribonuclease (RNase) treatment.
 Genome stores, propagates,
and express the genetic VP1 is responsible for viral
information that gives rise to a infectivity
cell's architectural and
functional machinery

VP2 participates in the receptor

recognition and in nuclear
translocation

Parvovirus B19 Viral Structure with Parts & Function

 02.
SURFACE ANTIGENS
SURFACE ANTIGENS
 03.
VIRAL PROTEINS
 NON STRUCTURAL PROTEIN 1 (NS1)

NS1 is 671 amino acid long protein that has a MW of ~78

kDa. NS1 contains two nuclear localization signals; KKPR
and KKCGKK (316–321) and is found predominantly in
the nucleus of infected cells. NS1 contains a DNA binding
and endonuclease domain at the N-terminus, an ATPase
and NTP-binding domains in the central region and a
transactivation domain at its C-terminus. NS1 is critical
for virus DNA replication and binds NSBEs (NS1 binding
elements) of the minimum origin of replication of B19V
dsRF DNA . Upon NS1 binding to NSBEs, it presumably
opens up the dsRF DNA and nicks the ssDNA substrate at
trs (terminal resolution site).
NON STRUCTURAL PROTEIN 1 (NS1)
With the assistance of Sp1/Sp3, NS1 binds P6
promoter for its transactivation. NS1 induces
apoptosis via NTP-binding motif (328-335 amino
acid) a DNA damage response and cell cycle arrest.
The putative transactivation domain 2 (TAD2) of
NS1 is critical for cell cycle arrest and the
transactivation of host genes. NS1 is thought to be
a global transactivator as the expression of NS1
protein in UT7/Epo-S1 affected around 1,770
genes, by upregulating 1,064 genes and
downregulating 706 GENES. In short, NS1 is a
multifunctional protein and plays various roles
during B19V infection
 11-kDa Protein
• The 11-kDa protein is expressed at high levels
during B19V infection and localizes more in the
cytoplasm than in the nucleus of infected cells.
The abundance of the 11-kDa protein in
infected cells is at least 100 times greater than
NS1 protein.

• The 11-kDa protein is potent inducer of

apoptosis during B19V infection and involves
caspase-10 We demonstrate that the 11-kDa
protein enhances viral DNA replication (~10-
fold), and thus determines virion production.
Finally, the 11-kDa protein has also been
implicated in VP2 production and its
distribution
 7.5-kDa Protein
• the 11-kDa protein has also been
implicated in VP2 production and
its distribution

• The function(s) of 7.5-kDa are still

unknown.
 04.
CORRELATIONS
 CARDIOVASCULAR AFFLICTION

• Numerous reports point B19V as a new cardiotropic virus

that may frequently cause acute inflammatory myocarditis (iMC)
which leads to DCM and isolated ventricular diastolic dysfunction.
B19V has been reported to infect intracardiac endothelial cells of
arterioles or venules which may impair microcirculation of the
myocardial cells besides owing to inflammatory cells penetration
into the myocardium and may cause ventricular dysfunction and
secondary myocyte necrosis.
 CARDIOVASCULAR AFFLICTION
• Further, genotypes 1 and 2 of B19V have been
commonly detected in endomyocardial tissues of
myocarditis (MC), while genotype 2 is more common
in iMC and in female. Active B19V infection in such
patients was documented by the finding of B19V-
mRNA replication intermediates; study at molecular
level showed B19V reactivation from latency and
induction of altered cardiac gene expression in a
subgroup of cardiomyopathy patients. Endothelial
cell regeneration may also be inhibited through
B19V-infected circulating angiogenic cells in patients
with DCM. B19V association in the pathogenesis of
MC and its progression towards MC/DCM remains
unproven.
 RENAL AFFLICTION
reported in a variety of clinical situations with
pathological lesions such as ;
 acute thrombotic microangiopathy
 Focal segmental glomerulosclerosis or
collapsing glomerulopathy
 post-infectious glomerulonephritis
 Endocapillary proliferative glomerulonephritis
 anemia in renal transplant recipients.
 RENAL AFFLICTION
Mechanisms involved ;
 causation of vasculitic changes in intra-renal
small- and medium-sized blood vessels
 production of cytopathic effects on glomerular
epithelial or endothelial cells
 massive deposition of immune complexes on
subendothelial cells

• result clinically in impaired immune responses,

deficient production of erythropoietin besides
decrease in erythrocyte survival
• 2% Renal transplant recipients get B19V
infection, other study it as high as 30%
 HEPATIC AFFLICTION
• liver infection by B19V – causative agent of
hepatitis or hepatitis with anemia

• as a sole causative agent in a few children with

acute viral hepatitis, but most children had
B19V co-infection along with other
hepatotropic viruses.

• B19V-induced hepatitis is under-recognized, it

may cause elevation of liver transaminases,
acute or chronic hepatitis and rarely
fulminant liver failure, macrophage activation
syndrome
 NEUROLOGIC AFFLICTION
• A systematic review on neurological involvement
of B19V-related infections included 129 patients,
of whom
79 (61.2%) had central nervous system
manifestations
41 (31.8%) had peripheral nervous system
manifestations
9 (7%) had encephalomyelitis, but most had
encephalitis (50/129)

• Several other neurological afflictions, acute

encephalitis and encephalopathy, focal seizure,
mononeuropathy multiplex, Guillain-Barré
syndrome have been reported, but the mechanism
is largely obscure

.
 NEUROLOGIC AFFLICTION
• molecular mimicry and autoimmunity to basic myelin
protein are most likely as in multiple sclerosis.

• Placental infection by B19V besides causing well-

documented non-immune hydrops faetalis, cause
fetal anemia and spontaneous abortions, congenital
infections and more serious placental abruptions.

• Gut infections due to B19V infection has been shown

to be localized in the intestinal mucosa and reported
to cause severe inflammatory bowel disease while
non-occlusive ischemic gangrene of stomach or bowel
caused by B19V
 HEMATOLOGIC AFFLICTION
• Hematological infections due to B19V presenting as
aplastic crisis were the first documented clinical
manifestation of this virus.

• B19V targets erythroid progenitor cells such as

erythroblast in the bone marrow and may causes
lytic infection resulting in severe anemia, PRCA
which may lead to myelodysplasia. Non-erythroid
cell infections by B19V involving platelets are
uncommon but may occur as some of the
thrombocytes are known to possess receptor for
B19V and thus cause thrombocytopenia with while
the report on acquired pure megakaryocytic
thrombocytopenia remains solitary.
 HEMATOLOGIC AFFLICTION
• Other afflictions such as macrophage
activation as in hemophagocytosis
syndrome induced by B19V are also rare.
Further, non-erythroid cell infections of
leucocytic cells by B19V include leucopenia
and agranulocytosis while more severe
disorders reported are pancytopenia, bone
marrow failures, aplastic anemia and necrosis
of bone marrow or fat embolism.
 HEMATOLOGIC AFFLICTION
• In leukemia especially in children with ALL, B19V
infection may precede or precipitate leukemia and
may also complicate the course of leukemia by
causing persistent anemia and requiring prolonged
duration of induction therapy.

• B19V has been proposed to cause leukemia through

methylation of cancer genes by anti-B19V IgG and
deficient production of IL-10 at birth.

• B19V may have a dual role, one in causation of

leukemia and second possession of natural
oncolytic property of B19V or controlling leukemia
and preventing deaths in children with ALL.
 CUTANEOUS AFFLICTION

• Cutaneous manifestations of B19V are uncommon and

varied from rash of erythema infectiosum to purpuric-
petechial eruption, pseudo-erysipelas and scleroderma.

• Mechanism is mostly due to immune complex mediated,

but B19V may directly infect endothelial cells as well as
fibroblasts in the skin with enhanced tumor necrosis
factor (TNF)-alpha expression and vascular deposition of
C5b-9 in the endothelial cells besides neoantigenicity and
cell injury as seen in scleroderma.
 CUTANEOUS AFFLICTION

• Recently, a four year old child with drug rash and

eosinophilia with systemic symptoms syndrome on
fluoxetine and complicated by B19V infection
 THANK
YOU!
Do you have any questions?
CREDITS: This presentation template was created
by Slidesgo, including icons by Flaticon, and
infographics & images by Freepik

Please keep this slide for attribution

 REFERENCES

• https://www.frontiersin.org/articles/10.3389/fcimb.2018.00166/full#:~:text
=Parvovirus%20B19%20(B19V)%20is%20a,et%20al.%2C%202017
).
• https://www.ncbi.nlm.nih.gov/books/NBK7715/
• https://www.uptodate.com/contents/microbiology-epidemiology-and-pathog
enesis-of-parvovirus-b19-infection