College of Medicine Microbiology Medical Virology dna viruses



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College of Medicine Microbiology

Medical Virology

DNA viruses( Herpesviruses): Dr.Jawad Kadhim Tarrad

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Epstein-Barr virus(EBV):

  • It has two types; EBV-1 and EBV-2.

Source and transmission:

  • Humans are natural host.

  • The virus is transmitted by oral secretion (exchange of saliva during kissing) . It also can transmitted by blood transfusion and organ transplantation.

Pathogenesis:

  • EBV initiates infection of epithelial cells of oropharynx and salivary glands, and spreads to cervical lymph nodes, then travels via blood to liver and spleen.

  • Mainly EBV infects and establishes latent infection in B-lymphocytes that persists for life.

Diseases and clinical pictures:

  • Primary infection is known as infectious mononucleosis(a.k.a: kissing disease or glandular fever). In young adults , after I.P : 30-50 days , I.M is characterized by fever ,pharyngitis sore throat, lethargy, fatigue ,headache ,malaise, lymphadenopathy ,splenomegaly , and elevated liver enzymes. The infection is usually resolving in 1-2 weeks. Most primary EBV infections in children are usually asymptomatic.

  • Recurrent infection is reactivated and closely linked with tumors (cancer). The EBV is oncogenic virus and related to Burkitt lymphoma (this disease is common in African children, especially who infected with malaria) , nasopharyngeal carcinoma (the disease is common in south Asia especially in males of Chinese origin, especially who eating salted fish that treated with nitrosamine), and Hodgkin lymphoma disease(common in Europe and Africa). EBV is also associated with X-linked lymphoproliferative syndrome , and hairy leukoplakia, a whitish lesion on tongue seen especially in AIDS patients.

Epidemiology:

  • EBV is distributed worldwide. It is common in all parts of world.

  • In developing countries. Infection occurs in early life; more than 90% of children are infected by age 6.

  • Over 90% of adults are seropositive for EBV.

  • Humans are only hosts of EBV. No animal reservoirs.



Lab. Dx :

  • EBV mononucleosis is diagnosed by demonstration of atypical lymphocytes (abnormal lymphocytes) in blood smear.

  • EBV-specific serologic tests (Paul-Bunnell test) can be used to detect heterophile antibodies that common in EBV infection.

  • The presence of IgM is indicative of current infection, while detection of IgG is marker of past infection and indicates immunity.

  • EBV DNA can be detected by PCR.

Control :

  • There is no specific antiviral therapy for EBV. Acyclovir has little activity against EBV.

  • There is no vaccine available to prevent infection.

  • Avoidance of contact with saliva and kissing children on mouth are important rules.



Cytomegalovirus(CMV):

Source and transmission:

  • Humans are the natural hosts. Whereas animal CMV strains do not infect human.

  • The virus is transmitted from person to person by several different ways.

    1. In early life, it is transmitted across placenta, within birth canal, and commonly in breast milk.

    2. In young children , its most common mode of transmission is via saliva.

    3. In adults, it is transmitted sexually, and it can also be transmitted during blood transfusion and organ transplants.

  • In other words, the virus is transmitted by contact with body fluids such as ; saliva, urine, semen, breast milk, cervical secretions , and blood.

Pathogenesis :

  • There are two clinical forms of CMV infection :

    1. Primary infection (congenital infection) .

    2. Re-infection(immunosuppressed individuals).

  • The virus initial replicate in epithelial cells of oropharynx especially in salivary (parotid) glands , it spreads to lymphoid tissues , and produces a viremia , then the virus disseminates systemically to involve multiple organs (liver ,kidney , spleen, lungs, brain). CMV remains latent in mononuclear cells and is reactivated in immunosuppressed patients.

  • Primary infection is called cytomegalic inclusion disease(CID) in neonates, which characterized by multinucleated giant cells with prominent intranuclear inclusion. Because giant cells are formed ,hence the name cytomegalo(enlargement of infected cell). Many organs are affected, and widespread congenital abnormalities result. Infection of fetus occurs in the pregnant women , ie, when she has no antibodies that will neutralize the virus before it can infect the fetus. Congenital abnormalities are more common when a fetus is infected during the first trimester than later in gestation.

  • CMV enters a latent state in leukocytes (monocytes) and T-cells, and can be reactivated when cell-mediated immunity is decreased .

Diseases and clinical features:

  • Congenital CMV-infection by this virus during gestation show clinically manifestations of cytomegalic inclusion disease(CID) such as microcephaly , hepatosplenomegaly ,seizure , deafness, jaundice, and purpura. CID is one of leading causes of mental retardation. Infected infants can continue to secrete CMV(shedding) in urine for several years. Primary infection of children and adults are usually asymptomatic.

  • Mononucleosis-like syndrome in older children and adults characterized by persistent fever ,pharyngitis, fatigue, malaise, and lymphadenopathy that is clinically similar to EBV-mononucleosis.

  • CMV-opportunistic infections. The virus is common cause pneumonia in immunosuppressed patients who have received transplants. It can causes retinitis(which can lead to blindness) in patients with AIDS, and also causes encephalitis and colitis.

Epidemiology:

  • CMV infection occur worldwide distribution. The endemic infection can occur in all parts of the world .

  • The natural hosts are humans, while animal viruses do not infect human.

  • CMV poses an important public health problem because of its high frequency of congenital infections, which may lead to severe congenital anomalies.

N.B:

Most common agents of congenital infections are collected in TORCHES term, acronym for Toxoplasma, Rubella, CMV, HSV-2, and syphilis.


Lab. Dx:

  • CMV can be isolated by cytopathic effects in cell culture.

  • Directed diagnosed by immunoflourescence test for detect CMV-specific antibodies. Detection of IgM antibody , indicative of current infection while detection of IgG suggests past infection.

  • CMV-DNA can be detected in body fluids by PCR.

Control:

  • Treatment: Ganciclovir is drug of choice for treatment of CMV infections, but the drug is highly toxic. Foscarnet is used to treat CMV infections resistant to ganciclovir.

  • Prevention:

  1. There is no vaccine available to prevent CMV infections. Now live vaccine and recombinant vaccine are under development.



  2. Barrier contraception and safe sex practice are important preventive measures.


Human herpes virus type-6 and type-7(HHV-6 and HHV-7):

  • Genus: Roseollavirus.

  • These herpes viruses are less common and less virulent.

Source and transmission:

  • Humans are natural host.

  • Transmission of HHV-6 and HHV-7 occurs by saliva secretion.

Pathogenesis and clinical findings:

  • Both viruses infect lymphoid tissues, T-cells (lymphotropic).

  • They have capacity to establish latent infection in lymphoid cells, T-lymphocytes.

  • Both viruses cause exanthema subitum (roseola infantum or sixth disease of rash) in children and is characterized by high fever for 2-5 days, followed by generalized maculopapular rash.

  • Infections persist for life. Reactivation of infection can occur in immunocompromised patients. Reactivation appears to be common in transplant patients and during pregnancy.

Lab.Dx:

  • Serologic tests are used to detect virus-specific IgM and IgG.

  • DNA of HHV-6 and HHV-7 can be detected by PCR.

Control :

  • Treatment : There is no specific antiviral therapy.

  • Prevention : There is no vaccine against these viruses.

Human herpes virus type-8(HHV-8)


  • HHV-8 is minor pathogen for human.

Source and transmission:

  • Humans are natural host.

  • Transmission of HHV-8 is by

    1. Sexual contact.

    2. Saliva exchange.

    3. Transplanted organs.

Pathogenesis and clinical findings:

  • HHV-8 infects B-lymphocytes and endothelial cells .

  • It establishes a latent infection in B cells.

  • The virus encodes many potentially oncogenic producers and cause Kaposi sarcoma (KS), a spindle cell of endothelial origin, characterized by lesions on skin, face, or oral cavity that appear as bruised or discolored spots and that progress to ulcerated nodules.

  • HHV-8 cause disease in rarely incidence in human.

  • Kaposi sarcoma-associated herpes virus is most common in patients with AIDS.

Lab. Dx:

  • Biopsy of skin lesions for detection of spindle cells.

  • HHV-8 infection is detected by PCR and hybridization.

Control :

Treatment:



  • There is no specific antiviral therapy .

  • Surgical excision or radiation.

  • Alpha interferon can be used.

Prevention :

  • There is no vaccine against this virus.

  • Safe sex practice should reduce the risk of transmission.









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