MICROBIOLOGY

Parvovirus, Papillomavirus, and Polyomavirus

Dr. Palacpac
PARVOVIRUS
 Smallest & simplest of all viruses
 SS (-) strand DNA; no virion polymerase; icosahedral; naked
 Virus Protein 2 (VP2) – major capsid protein
 Non Structural Proteins (NS-1) required for replication
 Highly resistant to inactivation
Since they are naked virus, they are resistant to inactivation by certain
factors like detergents, soap, pH, etc.
 Replicated only when a cell is in S phase
 Defective virus  requires a helper virus for replication (Herpes virus
or Adenovirus)
In order for them to cause an infection, they would need the help of another
virus such as Herpes virus and Adenovirus
Erythema Infectiosum (5th Disease)
 Children of early school age; occ. Adults
 Incubation Period: 1-2 weeks
 Viremia 1 week after infection  persist for 5 days  virus present
in nasal washes & gargle specimens
o Pharynx is the most probable site of viral shedding
 Biphasic  Lytic stage (contagious stage) & immunologic
 Generalized erythematous rash most important in the face 
“Slapped Cheek” appearance; lace-like rash on limbs or trunk
 Arthralgia (hands & knees) – adults

 PaRVo virus
o Human pathogen – B19  with tropism for RBC
progenitors

CLASSIFICATION
1. Parvovirinae
a) Genus Erythrovirus
 Parvovirus B19 (Type 1)
 Strain K71 (Type 2) Recently identified
 Strain V9 (Type 3) human genotypes Other Clinical Syndromes
b) Genus Bocavirus – newly discovered 1. Arthritis in adults – resembles RA (Rheumatoid Arthritis)
c) Genus Dependovirus 2. Pure Red Cell Aplasia
 AAV-2  defective virus  depend on a o Persistent infections and chronic anemia in
helper virus (Adenovirus or Herpes virus) for immunocompromised patients
replication 3. Hydrops Fetalis
2. Densovirinae – infect insects o Result of severe fetal anemia, especially in 2nd trimester
 CHF
B-19 VIRUS  Fetal death before 20th week of pregnancy
 Only member – cause infections in humans o No congenital abnormalities
 Cellular receptor: blood group P antigen (mature erythrocytes,
endothelial cells, placenta, megakaryocytes, fetal liver, heart) Human Bocavirus Respiratory Infection
 Has tropism for:  Prevalent in children with acute wheezing
1) Erythroblasts in Bone Marrow  aplastic anemia  Often found in mixed infections with other viruses
2) Endothelial cells in blood vessels  rashes  Pathogenesis unknown
 MOT:  MOT: probable respiratory route; also detected in stool and serum
1) Respiratory route – primary samples
2) Blood transfusion
3) Vertical/transplacental transmission LABORATORY DIAGNOSIS
 Most sensitive tests detect viral DNA  PCR (most sensitive), in situ
 No evidence of virus excretion in feces or urine hybridization of fixed tissue
 Humans – natural reservoir  Serology:
 Principal targets: immature cells in erythroid lineage (erythroblasts) o B19 IgM antibody – recent infection; present 2-3 months
 Replication  death of infected cells  cessation of RBC production after infection

5th Disease: TREATMENT

 Symptomatic
 Transient aplastic crisis: symptomatic; may require blood transfusion
 Ig preparations containing neutralizing antibodies for
immunocompromised & those with anemia

PREVENTION
 No vaccine
 Good hygiene
 Standard infection control practices for health workers

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 MICROBIOLOGY
Parvovirus, Papillomavirus, and Polyomavirus
Dr. Palacpac
PAPILLOMAVIRUS/POLYOMAVIRUS Picture on Lower Left:
 Causes lytic, chronic, latent & transforming infections depending host They would replicate initially at the basal epithelial cells, whether be in your
cell cervix, uterus, penis, etc. They would first invade the basal cells of these areas
 Small, icosahedral capsid, non-enveloped, dsDNA genomes that would give rise to a latent infection (no virus infection) then later it would
migrate to the upper portions of the skin that would give rise to cell
proliferation and other group of oncogenes directly to the surface of the
1. Early Genes (E1-E7)
epithelium that would cause the assembly of these virus and the release of
o Facilitate replication of viral genome codes for non-
these virus on the surface
structural protein
Modes of Transmission:
2. Late Genes (L1 & L2)
1. Direct contact
o Viral attachment protein
2. Minor skin abrasions
o Codes for structural protein
3. Sexual contact
4. Vertical transmission
HUMAN PAPILLOMAVIRUS (HPV)
 Former members of Papovaviridae Clinical Infections:
 ds circular DNA, icosahedral, naked 1. Skin warts  serotypes 1 to 4
 Oncogenic  E6 & E7 oncoproteins 2. Laryngeal papillomas  serotypes 6 &11
 Do not grow in cell culture 3. Anogenital warts (condylomata acuminata)  6 & 11
 Capsomere form regular pointed star-shaped head 4. Cervical, oropharyngeal & penile CA  16 & 18
 Tissue tropism  epithelial cells of skin & mucous membranes 5. Epidermodysplasia verruciformis
 Encode 7 early genes (E1-E7) & 2 late structural genes (L1 & L2) 
bind with growth suppressor proteins
o E6 protein binds to p53
o E7 protein binds to p105RB
 In permissive cells  cause lytic infections
 In non-permissive cells  abortive, latent, persistent, immortalizing
infections
 Important characteristics:
o Stimulate cell DNA Synthesis
o Significant cause of human cancer
o Viral oncoproteins interact with cellular tumor
suppressor genes

Classification of HPV:
 Alpha papillomavirus
 Beta papillomavirus Laboratory Diagnosis:
 Gamma papillomavirus 1. Cytology
 Mupapapillomavirus 2. DNA molecular probe
 Napapapillomavirus 3. PCR
4. Southern Blot
Pathogenesis:
 Infect & replicate in squamous epithelium of skin (warts) or mucous Treatment:
membrane (papillomas) 1. Removal of the lesion
 Recurrence is common o Surgical excision, Application of caustic agents
 Innate immunity & CMI are important in resolution and control of o Cryosurgery
infections o Electrocautery
o Laser therapy

2. Anti-HPV drugs or immunomodulating drugs

o Imiquimod
o Topical idoxuridine
o Systemic or intralesional alpha interferon
o Cidofovir

Prevention:
 Quadrivalent & Bivalent HPV vaccine – given to 9-54 yrs of age
o Contains virus-like particles composed of HPV L1 proteins
o Quadrivalent – from HPV types 6, 11, 16, and 18
o Bivalent – from HPV types 16 and 18

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 MICROBIOLOGY
Parvovirus, Papillomavirus, and Polyomavirus
Dr. Palacpac
POLYOMAVIRUSES Merkel Cell Polyomavirus (2008)
 Formerly part of Papovaviridae (no longer exists)  share many  Merkel cell carcinomas – skin tumor of neuroendocrine origin
similarities with Papillomaviridae
 Transforming capabilities SV40 Virus
 Circular, dsDNA genome; icosahedral; naked  Fecal-oral route
 Genome with 2 regions:  DNA detected in brain tumors, mesotheliomas, bone tumors &
1) Early region – necessary for replication of viral DNA in lymphomas
permissive cells
2) Late region – for synthesis of coat protein NOTE from Doc Palacpac:
1. Know the morphological differentiation and characteristics
 Stimulate viral oncoproteins interaction with cellular tumor 2. Know the different manifestations
suppressor proteins 3. Know the different serotypes and the carcinomas that they cause
 Important model tumor virus 4. Know the MOT
5. Know the different diseases associated with each virus
 May cause human cancer
REFERENCES
Polyomaviruses:
1. BK Virus  PPT
o Acute hemorrhagic cystitis in bone marrow transplant  Microbiology Manual (2019)
patients & ureteral stenosis  Dr. Palacpac Recordings

2. JC Virus
o Progressive Multifocal Leukoencephalopathy 
destruction of oligodendrocytes; possible role in
colorectal cancer

3. Simian 40 Virus  animal pathogen

BK and JC Viruses
 Usually early childhood
 May persist in kidneys, lymphoid tissues of healthy individuals
 JC virus associated with human brain tumors

KI and WU Viruses
 Discovered in 2007 in nasopharyngeal aspirates from children with
respiratory infections
 Widespread, occur likely in childhood

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