Herpse Viruses

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Herpse Viruses

• Xiao-Kui GUO
• Dept. of Microbiology and Parasitology

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BIOLOGICAL PROPERTIES
Virion Spherical, 150-200 nm in diameter (icosahedral)
Genome Double-stranded DNA, linear, 124235 kbp, reiterated sequences
Proteins More than 35 proteins in virion
Envelope  Contains viral glycoproteins, Fc receptors
Replication Nucleus, bud from nuclear membrane
Outstanding characteristics Encode many enzymes
Establish latent infections
Persist indefinitely in infected hosts
Frequently reactivated in immunosuppressed hosts
Some are cancer-causing
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Structure Composition

• Size 150-200nm.
• Enveloped double stranded DNA viruses.
• Capsid icosahedral symmetry and has 162
  capsomeres.
• Nucleocapsid surrounded by an envelope contains
  viral glycoprotein spikes about 8 nm long.
• Genome Large and encodes at least 100 different
  proteins.

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Classification
Subfamily (-herpesvirinae) Biologic Properties Biologic Properties Genus (-virus) Examples Examples
Subfamily (-herpesvirinae) Growth Cycle and Cytopathology Latent Infections Genus (-virus) Official Name (Human herpesvirus) Common Name
Alpha Short, cytolytic Neurons Simplex 1 Herpes simplex virus type 1
Alpha Short, cytolytic Neurons Simplex 2 Herpes simplex virus type 2
Alpha Short, cytolytic Neurons Varicello 3 Varicella-zoster virus
Beta Long, cytomegalic Glands,kidneys Cytomegalo 5 Cytomegalovirus
Beta Long, lympho- proliferative Lymphoid tissue Roseolo 6 Human herpesvirus 6
Beta Long, lympho- proliferative Lymphoid tissue Roseolo 7 Human herpesvirus 7
Gamma Variable, lympho- proliferative Lymphoid tissue Lymphocrypto 4 Epstein-Barr virus
Gamma Variable, lympho- proliferative Lymphoid tissue Rhadino 8 Kaposis sarcomaassociated herpesvirus
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Herpesvirus Replication
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Herpes Simplex Viruses
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Properties

• Belong to the alphaherpesvirus subfamily of
  herpesviruses
• Double stranded DNA enveloped virus with a genome
  of around 150 kb
• The genome of HSV-1 and HSV-2 share 50 - 70
  homology.
• They also share several cross-reactive epitopes
  with each other. There is also antigenic
  cross-reaction with VZV.
• Man is the only natural host for HSV.

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Epidemiology (1)

• HSV is spread by contact, as the virus is shed in
  saliva, tears, genital and other secretions.
• By far the most common form of infection results
  from a kiss given to a child or adult from a
  person shedding the virus.
• Primary infection is usually trivial or
  subclinical in most individuals. It is a disease
  mainly of very young children ie. those below 5
  years.
• There are 2 peaks of incidence, the first at 0 -
  5 years and the second in the late teens, when
  sexual activity commences.
• About 10 of the population acquires HSV
  infection through the genital route and the risk
  is concentrated in young adulthood.

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Epidemiology (2)

• Generally HSV-1 causes infection above the belt
  and HSV-2 below the belt. In fact, 40 of
  clinical isolates from genital sores are HSV-1,
  and 5 of strains isolated from the facial area
  are HSV-2. This data is complicated by oral
  sexual practices.
• Following primary infection, 45 of orally
  infected individuals and 60 of patients with
  genital herpes will experience recurrences.
• The actual frequency of recurrences varies widely
  between individuals. The mean number of episodes
  per year is about 1.6.

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Epidemiology

• Worldwide in distribution.
• No animal reservoirs or vectors.
• Transmission is by contact with infected
  secretions.
• The epidemiology of type 1 and type 2 herpes
  simplex virus differs.

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Pathogenesis

• During the primary infection, HSV spreads locally
  and a short-lived viraemia occurs, whereby the
  virus is disseminated in the body. Spread to the
  to craniospinal ganglia occurs.
• The virus then establishes latency in the
  craniospinal ganglia.
• The exact mechanism of latency is not known, it
  may be true latency where there is no viral
  replication or viral persistence where there is a
  low level of viral replication.
• Reactivation - It is well known that many
  triggers can provoke a recurrence. These include
  physical or psychological stress, infection
  especially pneumococcal and meningococcal, fever,
  irradiation including sunlight, and
  menstruation.

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Immunity

• Transplacentally (????) acquired antibodies.
• HSV-1 antibodies- Appear in early childhood.
• HSV-2 antibodies-Rise during the age of
  adolescence and sexual activity.
• Primary infections-IgM antibodies appear
  transiently and are followed by IgG and IgA
  antibodies that persist for long periods.
• Latent state- Antibodies can modify subsequent
  disease.

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Clinical Manifestations

• HSV is involved in a variety of clinical
  manifestations which includes -
• 1. Acute gingivostomatitis???
• 2. Herpes Labialis (cold sore)
• 3. Ocular Herpes
• 4. Herpes Genitalis
• 5. Other forms of cutaneous herpes
• 7. Meningitis
• 8. Encephalitis
• 9. Neonatal herpes

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Oral-facial Herpes

• Acute Gingivostomatitis
• Acute gingivostomatitis is the commonest
  manifestation of primary herpetic infection.
• The patient experiences pain and bleeding of the
  gums. 1 - 8 mm ulcers with necrotic bases are
  present. Neck glands are commonly enlarged
  accompanied by fever.
• Usually a self limiting disease which lasts
  around 13 days.
• Herpes labialis (cold sore)
• Following primary infection, 45 of orally
  infected individuals will experience
  reactivation. The actual frequency of recurrences
  varies widely between individuals.
• Herpes labialis (cold sore) is a recurrence of
  oral HSV.
• A prodrome of tingling, warmth or itching at the
  site usually heralds the recurrence. About 12
  hours later, redness appears followed by papules
  and then vesicles.

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Ocular Herpes

• HSV causes a broad spectrum of ocular disease,
  ranging from mild superficial lesions involving
  the external eye, to severe sight-threatening
  diseases of the inner eye. Diseases caused
  include the following-
• Primary HSV keratitis dendritic ulcers
• Recurrent HSV keratitis
• HSV conjunctivitis
• Iridocyclitis, chorioretinitis and cataract

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Genital Herpes

• Genital lesions may be primary, recurrent or
  initial.
• Many sites can be involved which includes the
  penis, vagina, cervix, anus, vulva, bladder, the
  sacral nerve routes, the spinal and the meninges.
  The lesions of genital herpes are particularly
  prone to secondary bacterial infection eg.
  S.aureus, Streptococcus, Trichomonas and Candida
  Albicans.
• Dysuria is a common complaint, in severe cases,
  there may be urinary retention.
• Local sensory nerves may be involved leading to
  the development of a radiculitis. A mild
  meningitis may be present.
• 60 of patients with genital herpes will
  experience recurrences. Recurrent lesions in the
  perianal area tend to be more numerous and
  persists longer than their oral HSV-1
  counterparts.

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• Genital herpes.

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Herpes Simplex Encephalitis

• Herpes Simplex encephalitis is one of the most
  serious complications of herpes simplex disease.
  There are two forms
• Neonatal there is global involvement and the
  brain is almost liquefied. The mortality rate
  approaches 100.
• Focal disease the temporal lobe is most
  commonly affected. This form of the disease
  appears in children and adults. It is possible
  that many of these cases arise from reactivation
  of virus. The mortality rate is high (70)
  without treatment.
• It is of utmost importance to make a diagnosis of
  HSE early. It is general practice that IV
  acyclovir is given in all cases of suspected HSE
  before laboratory results are available.

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Neonatal Herpes Simplex (1)

• Incidence of neonatal HSV infection varies
  inexplicably from country to country e.g. from 1
  in 4000 live births in the U.S. to 1 in 10000
  live births in the UK
• The baby is usually infected perinatally during
  passage through the birth canal.
• Premature rupturing of the membranes is a well
  recognized risk factor.
• The risk of perinatal transmission is greatest
  when there is a florid primary infection in the
  mother.
• There is an appreciably smaller risk from
  recurrent lesions in the mother, probably because
  of the lower viral load and the presence of
  specific antibody
• The baby may also be infected from other sources
  such as oral lesions from the mother or a
  herpetic whitlow in a nurse.

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Neonatal Herpes Simplex (2)

• The spectrum of neonatal HSV infection varies
  from a mild disease localized to the skin to a
  fatal disseminated infection.
• Infection is particularly dangerous in premature
  infants.
• Where dissemination occurs, the organs most
  commonly involved are the liver, adrenals and
  the brain.
• Where the brain is involved, the prognosis is
  particularly severe. The encephalitis is global
  and of such severity that the brain may be
  liquefied.
• A large proportion of survivors of neonatal HSV
  infection have residual disabilities.
• Acyclovir should be promptly given in all
  suspected cases of neonatal HSV infection.
• The only means of prevention is to offer
  caesarean section to mothers with florid genital
  HSV lesions.

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Other Manifestations

• Disseminated herpes simplex are much more likely
  to occur in immunocompromised individuals. The
  widespread vesicular resembles that of
  chickenpox. Many organs other than the skin may
  be involved e.g. liver, spleen, lungs, and CNS.
• Other cutaneous manifestations include
• eczema herpeticum which is potentially a serious
  disease that occurs in patients with eczema.
• Herpetic whitlow which arise from implantation of
  the virus into the skin and typically affect the
  fingers.
• zosteriform herpes simplex". This is a rare
  presentation of herpes simplex where HSV lesions
  appear in a dermatomal distribution similar to
  herpes zoster.

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Laboratory Diagnosis

• Direct Detection
• Electron microscopy of vesicle fluid - rapid
  result but cannot distinguish between HSV and VZV
• Immunofluorescence of skin scrappings - can
  distinguish between HSV and VZV
• PCR - now used routinely for the diagnosis of
  herpes simple encephalitis
• Virus Isolation
• HSV-1 and HSV-2 are among the easiest viruses to
  cultivate. It usually takes only 1 - 5 days for a
  result to be available.
• Serology
• Not that useful in the acute phase because it
  takes 1-2 weeks for before antibodies appear
  after infection. Used to document to recent
  infection.

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Cytopathic Effect of HSV in cell culture Note
the ballooning of cells. (Linda Stannard,
University of Cape Town, S.A.)
Positive immunofluorescence test for HSV antigen
in epithelial cell. (Virology Laboratory,
New-Yale Haven Hospital)
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Management

• At present, there are only a few indications of
  antiviral chemotherapy, with the high cost of
  antiviral drugs being a main consideration.
  Generally, antiviral chemotherapy is indicated
  where the primary infection is especially severe,
  where there is dissemination, where sight is
  threatened, and herpes simplex encephalitis.
• Acyclovir???? this the drug of choice for most
  situations at present. It is available in a
  number of formulations-
• I.V. (HSV infection in normal and
  immunocompromised patients)
• Oral (treatment and long term suppression of
  mucocutaneous herpes and prophylaxis of HSV in
  immunocompromised patients)
• Cream (HSV infection of the skin and mucous
  membranes)
• Ophthalmic ointment
• Famciclovir and valacyclovir oral only, more
  expensive than acyclovir.
• Other older agents e.g. idoxuridine,
  trifluorothymidine, Vidarabine (ara-A).
• These agents are highly toxic and is suitable
  for topical use for opthalmic infection only

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Varicella-Zoster Virus
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Biological Properties

• Morphologically identical to herpes simplex
  virus.
• Cause chickenpox and zoster.
• Cross-protection between zoster and varicella.

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Pathogenesis Pathology

• Varicella
• The route of infection is the mucosa of the
  upper respiratory tract or the conjunctiva.
• Primary viremia and secondary viremia
• Zoster
• Distribution of lesions in the skin corresponds
  closely to the areas of innervation (????) from
  an individual dorsal root ganglion (????).

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Pathogenesis
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Clinical findings
Rash of Chickenpox
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Zoster
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Immunity

• Antibodies induced by varicella vaccine persist
  for at least 20 years.
• Zoster occurs in the presence of neutralizing
  antibody to varicella.

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Laboratory Diagnosis

• Immunofluorescence staining.
• Isolation and Identification of Virus.
• Serology

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Epidemiology

• Varicella and zoster occur worldwide.
• Varicella-A common epidemic disease of childhood.
• Zoster- sporadically, chiefly in adults.

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Treatment Prevention

• Varicella required no treatment in normal
  children.
• Gamma globulin of high varicella-zoster virus
  antibody titer.
• Several antiviral compounds.
• Live attenuated (?????) varicella vaccine.

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Cytomegalovirus
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Biological Properties

• The largest genetic content of the human
  herpesviruses.
• ds DNA enveloped virus
• Species-specific and cell type-specific.
• Intranuclear inclusion body and multinucleated
  cells.

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Pathogenesis Pathology

• Normal Hosts
• Immunosuppressed Hosts
• Congenital and Perinatal Infections

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Pathogenesis of CMV infections
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Immunity

• Cytomegalovirus-specific IgM, IgA, and IgG
  antibodies.
• Antibody in breast milk does not prevent
  transmission of infection to breast-feeding
  infants.

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Laboratory Diagnosis

• PCR and Antigen Detection Assays
• Isolation of Virus
• Serology

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CMV pp65 antigenaemia test
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Epidemiology

• Endemic in all parts of the world.
• Transmission requires close person-to-person
  contact.

Incidence of Cytomegalic Disease
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Treatment Control

• Ganciclovir (????), foscarnet (???), and
  acyclovir.
• Live and recombinant cytomegalovirus vaccines.

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Epstein-Barr Virus
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Biological Properties

• Biology of EBV
• Viral Antigens
• Latent phase antigens-EBNAsEBV (???)
• -LMPs
  (???????)
• Early antigens -nonstructural proteins.
• Late antigens -viral capsid antigen (??????)
  and viral envelope.
• Experimental Animal Infections.

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Pathogenesis Pathology

• Primary Infection
• Reactivation from Latency
• Tumors

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Infectious Mononuclosis

• Primary EBV infection is usually subclinical in
  childhood. However in adolescents and adults,
  there is a 50 chance that the syndrome of
  infectious mononucleosis (IM) will develop.
• IM is usually a self-limited disease which
  consists of fever, lymphadenopathy and
  splenomegaly. In some patients jaundice may be
  seen which is due to hepatitis. Atypical
  lymphocytes are present in the blood.
• Complications occur rarely but may be serious
  e.g. splenic rupture, meningoencephalitis, and
  pharyngeal obstruction.
• In some patients, chronic IM may occur where
  eventually the patient dies of lymphoproliferative
  disease or lymphoma.
• Diagnosis of IM is usually made by the heterophil
  antibody test and/or detection of EBV IgM.
• There is no specific treatment.

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Burkitts Lymphoma (1)

• Burkitt's lymphoma (BL) occurs endemically in
  parts of Africa (where it is the commonest
  childhood tumour) and Papua New Guinea. It
  usually occurs in children aged 3-14 years. It
  respond favorably to chemotherapy.
• It is restricted to areas with holoendemic
  malaria. Therefore it appears that malaria
  infection is a cofactor.
• Multiple copies of EBV genome and some EBV
  antigens can be found in BL cells and patients
  with BL have high titres of antibodies against
  various EBV antigens.

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Burkitts Lymphoma (2)

• BL cells show a reciprocal translocation between
  the long arm of chromosome 8 and chromosomes 14,
  2 or 22.
• This translocation result in the c-myc oncogene
  being transferred to the Immunoglobulin gene
  regions. This results in the deregulation of the
  c-myc gene. It is thought that this
  translocation is probably already present by the
  time of EBV infection and is not caused by EBV.
• Sporadic cases of BL occur, especially in AIDS
  patients which may or may not be associated with
  EBV.
• In theory BL can be controlled by the eradication
  of malaria (as has happened in Papua New Guinea)
  or vaccination against EBV.

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Nasopharyngeal Carcinoma

• Nasopharyngeal carcinoma (NPC) is a malignant
  tumour of the squamous epithelium of the
  nasopharynx. It is very prevalent in S. China,
  where it is the commonest tumour in men and the
  second commonest in women.
• The tumour is rare in most parts of the world,
  though pockets occur in N. and C. Africa,
  Malaysia, Alaska, and Iceland.
• Multiple copies of EBV genome and EBV EBNA-1
  antigen can be found in cells of undifferentiated
  NPC. Patients with NPC have high titres of
  antibodies against various EBV antigens.
• Besides EBV there appears to be a number of
  environmental and genetic cofactors in NPC.
• NPC usually presents late and thus the prognosis
  is poor.
• In theory NPC can be prevented by vaccination.

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Immunocompromised Patients

• After primary infection, EBV maintains a steady
  low grade latent infection in the body. Should
  the person become immunocompromised, the virus
  will reactivate. In a few cases,
  lymphoproliferative lesions and lymphoma may
  develop. These lesions tend to be extranodal and
  in unusual sites such as the GI tract or the CNS.
• Transplant recipients e.g. renal - EBV is
  associated with the development of
  lymphoproliferative disease and lymphoma.
• AIDS patients - EBV is associated with oral
  leukoplakia and with various Non-Hodgekins
  lymphoma.
• Ducan X-linked lymphoproliferative syndrome -
  this condition occurs exclusively in males who
  had inherited a defective gene in the
  X-chromosome . This condition accounts for half
  of the fatal cases of IM.

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Clinical Findings

• Infectious mononucleosis
• Several types of cancer

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Infectious mononucleosis
Burkitt's Lymphoma
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Immunity
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Laboratory Diagnosis

• Isolation and Identification of Virus.
• Serology

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Epidemiology

• Endemic in all around the world.
• Transmitted primarily by contact with
  oropharyngeal secretions.

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Prevention, Treatment Control

• No EBV vaccine available.
• Acyclovir

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Human Herpse Virus 6

• Worldwide
• In the saliva of the majority of adults (gt90).
• It infects almost all children by the age of two
  and the infection is life-long. Again, it
  replicates in B and T lymphocytes,
  megakaryocytes, etc
• Latent infection in T cells . Infected cells are
  larger than normal with inclusions in both
  cytoplasm and nucleus.

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Roseala Infantum
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Human Herpse Virus 7

• This virus binds to the CD4 antigen and
  replicates in T4 (CD4) cells and is found in the
  saliva of the majority of the adult population
  (gt75).
• Most people acquire the infection as children and
  it remains with them for the rest of their lives.
  It is similar to HHV-6 and may be responsible for
  some cases of exanthem subitum

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Human Herpse Virus 8

• Kaposis sarcoma-associated herpesvirus (KSHV)
  (?????????)
• Sexually transmitted.
• PCR, serology, indirect immuno-fluorescence,
  Western blot, and ELISA.
• Foscarnet, ganciclovir, and cidofovir.

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Kaposis Sarcoma
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Flavivirus

• Xiao-Kui GUO
• Dept. of Microbiology and Parasitology

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Flavivirus (???)

• A group of viruses of vertebrates biologically
  transmitted by hematophagous arthropod vectors
  (??????) from one vertebrate host (??????) to
  another and are therefore termed arboviruses
  (arthropod-borne viruses) .
• In our country, Japanese B encephalitis virus
  (??B????), Dengue virus (????), Forest
  encephalitis virus (??????).

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Common features

1. Spherical viruses about 20nm70nm in diameter
2. Single plus-stranded RNA with an icosahedral
   capsid surrounded by lipid envelope with spike of
   hemagglutinin (HA)
3. Labile to heat, lipolytic reagen, sodium
   desoxycholate, being readily inactivated at pH
   35 and room temperature, ether and other lipid
   solvents.
4. Flaviviruses replicate in the cytoplasm?
5. Arthropods serve as viral transmissible mediums
   and reservoir host.

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Clinical manifestations

1. Encephalitis or encephalomyelitis epidemic type
   B encephalitis, tick-borne encephalitis.
2. Systemic infection without any specific site,
   such as Dengue fever.
3. Systemic infection with major manifestation of
   hepatitis, such as yellow fever.
4. Systemic infection with major manifestation of
   hemorrhagic fever, such as Xinjiang HF.
5. Systemic infection with major manifestation of
   arthritis, such as Ross river fever.

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Scientist collecting specimens from trapped
rodents
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Arthropod Vectors
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Japanese B encephalitis virus

• Also called epidemic type B encephalitis virus
  (?????????), encephalitis B virus.
• First isolated by Japanese researchers.

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Biological Properties

• Belongs to Flavivirus.
• Small spherical enveloped virus, ssRNA genome
• SP C M E(HA)
• Replicates in susceptible animals, embryo eggs
  and cell culture
• Stable antigenicity
• Sensitive to lipid solvent agents, physical and
  chemical treatments.

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Epidemiology
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• Vector Culex tritaeniorhynchus (?????).
• Reserviors Young pigs.

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Pathogenesis
Systemic symptoms
Mosquito stings
Multiplication occurs in lymphoid cells or in
vascular endothelium
Initial viremia
Replication in cells of the monocyte-macrophage
system
Secondary viremia
Passes the blood-brain barrier
Infect nerve cells
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Immunity

• Both humoral immunity and cellar immunity are
  elicited and are important.
• The antibody blocks the viremia spread of the
  virus and the subsequent infection of other
  tissues.
• Lifelong immunity.

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Clinical findings
Sudden onset of fever ,headache and neck
stiffness. ??????????? Nausea or vomiting
?Convulsion?coma. ????? ?????? Rigidity or
weakness of the limbs. ???????
fatality rates often exceeding 20. ??????20 A
high percentage of survivors left
with neurologic and psychiatric sequelas.
?????????????????
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Laboratory Diagnosis

• Isolation and cell culture
• Serology Hemagglutination inhibition, ELISA, and
  latex agglutination or neutralization tests.
• RT-PCR

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Treatment and Prevention

• Mosquito control.
• Live attenuated vaccine or an inactivated vaccine.

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Dengue virus
Dengue virus is a causative agent of dengue fever
which is an acute infectious disease transmitted
by Aedes.
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Virus is circularly transmitted among the
mosquitohumanmosquito
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Clinical findings

• Most infections are asymptomatic?
• Dengue fever???
• high fever,headache,rash,and back and bone pain
• dengue hemorrhagic fever (DHF)????? and dengue
  shock syndrome (DSS)???????
• (antibody-dependent enhancement) ADE/immune
  enhancement?????????

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A large subcutaneous haemorrhage on the upper arm
of a patient with dengue haemorrhagic fever.
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Russian spring-summer encephalitis virus (RSSE)
This virus is one of flaviviridae and cause
tick-borne encephalitis
IXodid tick
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Epidemiology
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Hemorrhagic fever viruses

• Hemorrhagic fever viruses can cause the
  hemorrhagic fever and are transmitted by
  arthropods and rodents.
• Classified into the toga-,flavi-,bunya-(???),aren
  a- (??), and filovirus groups.
• Hantaan virus, Crimean-Congo hemorrhagic fever
  virus (????-???????), and Dengue virus.

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Reservoirs/vectors of viruses
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Hantavirus
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Biological Properties

• Bunyaviridae (??????).
• Spherical, enveloped particles 90 to 120 nm in
  diameter and contain single-stranded RNA.
• Glycoproteins (G1 and G2).
• Six serotypes of hantaviruses, ?? types. In
  china, ?? types.

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Pathogenesis and Immunity

• The virus infections in rodents are lifelong and
  without deleterious effects.
• Renal syndrome (HFRS) (???????)
• Hantavirus pulmonary syndrome (HPS) (????????)

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Epidemiology
Annualized average incidence of HFRS in mainland
China during 1994 1998.
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Crimean-Congo (xin-jiang) hemorrhagic fever virus

• Nairovius (?????) of Bunyaviridae
• Natural reservoirs

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RABIES VIRUS, PAPILLOMAVIRUSES, POXVIRUSES AND
HUMAN PARVOVIRUS B19

• Xiao-Kui GUO
• Dept. of Microbiology and Parasitology

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Rabies virus
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Biological Properties

• Rhabdoviridae (?????), Lyssavirus (??????).
• SsRNA, enveloped virus
• Wide host range.
• Single serotype

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Pathogenesis and Immunity

• Spread through nerve system.
• Negri body
• Acute, fatal encephalitis (?????).
• The clinical spectrum (???) can be divided into
  three phases.

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Negri body
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Epidemiology
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Treatment and Prevention

• No successful treatment for clinical rabies.
• Killed-virus vaccine is administered
  intramuscularly on the day of exposure and the on
  days 3,7,14,and 28.

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PAPILLOMAVIRUSES
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Biological Properties

• Papovaviridae family
• 55 nm in diameter.
• Double-stranded DNA enclosed within a
  nonenveloped capsid.
• Artificial cultivation un-successful.

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Pathogenesis and Immunity

• Highly tropic (?????) for epithelial cells of the
  skin and mucous membranes.
• HPV type 16 and 18 are considered to be high
  cancer risk.
• Cell-mediated immunity.

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LIFE CYCLE OF HUMAN PAPILLOMAVIRUS
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Oral Warts
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POXVIRUSES (???)

• The largest and most complex of viruses.
• All natural human poxvirus infections except
  molluscum are zoonoses and are geographically
  restricted.
• Variola virus (VV) and vaccinia are the best
  known.
• Vaccination history.

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Variola major (smallpox) of humans (a),
ectromelia virus (mousepox) of mice (b) or
camelpox virus of camels (c)
Viral Images
Smallpox vaccination
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HUMAN PARVOVIRUS B19

• The simplest DNA animal viruses.
• Parvovirus B19 has a tropism for erythroid
  progenitor cells (???????????).
• Transmission is presumably by the respiratory
  route, can also transmitted by blood transfusions
  or by infected blood products and vertically from
  mother to fetus.

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Erythema infectiosum, poly-arthralgia-arthritis
syndrome in normal adults, aplastic crisis in
patients with hemolytic disorders, chronic
anemia in immunocompromised individuals.
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PRION

• Xiao-Kui GUO
• Dept. of Microbiology and Parasitology

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Biological Properties

• Lacks detectable nucleic acids
• PrPsc (scrapie prion protein ????????)
• PrPc(cellular prion protein ??????).
• Unusually resistant to standard means of
  inactivation.

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Pathogenesis and Immunity
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Clinical findings

• Scrapie.
• Bovine Spongiformorm Encephalopathy and New
  Variant Creutzfeldt - Jakob disease.
• Kuru and Classic Creutzfeldt - Jakob disease.
• Chronic Wasting Disease.

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Laboratory Diagnosis

• Clinical grounds
• Histology
• Western blot

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Treatment and Prevention

• No treatment exists.
• Autoclaving
• 5 hypochlorite solution (???) or 1.0 M sodium
  hydroxide (????).

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