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Sexually Transmitted Viral Infections:. The most common viral causes are: Herpes simplex virus type 2 ( HSV-2 ) Human papillomavirus ( HPV ) Human immunodeficiency virus ( HIV ) Human cytomegalovirus ( HCMV ) Hepatitis B virus ( HBV ) Molluscum contagiosum virus ( MCV ).

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sexually transmitted viral infections

Sexually Transmitted Viral Infections:

The most common viral causes are:

Herpes simplex virus type 2 (HSV-2)

Human papillomavirus (HPV)

Human immunodeficiency virus (HIV)

Human cytomegalovirus (HCMV)

Hepatitis B virus (HBV)

Molluscumcontagiosum virus (MCV)

herpesviridae family


Icosahedral, enveloped double stranded DNA viruses.

Genome consists of long and short fragments which may be orientated in either direction, giving a total of 4 isomers.

Three subfamilies:

Alphaherpesviruses: HSV-1, HSV-2, VZV

Betaherpesviruses: CMV, HHV-6, HHV-7

Gammaherpesviruses: EBV, HHV-8

Set up latent or persistent infection following primary infection

Reactivation are more likely to take place during periods of immunosuppression.

herpes virus particle

Herpes virus Particle

HSV-2 virus particle

Note that all herpesviruses

have identical morphology

and cannot be distinguished

from each other under

electron microscopy

herpes simplex virus type 2 hsv 2

Herpes Simplex Virus Type 2 (HSV-2):

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.

Man is the only natural host for HSV.

Transmission of HSV-2 by:

Sexual contact, or

Infection during birth.



Primary infections commonly asymptomatic; Symptomatic cases sometimes severe, prolonged, systemic manifestations:

Fever - Malaise - Myalgia

Local pain - Itching

Painful vesiculoulcerative lesions: on the vulva, cervix and vagina or the penis.

Latency of HSV-2 is in sacral ganglia

Reactivation often asymptomatic.

Takes place during sexual intercourse.

Manifest at any site innervated by the affected neurons.

hsv 2 diseases

HSV-2 Diseases:

Herpes genitalis: -The classical presentation. - Extensive bilateral painful vesicular lesions in the genital area, accompanied with fever, dysuria and inguinal lymphadenopathy.

Neonatal herpes: -The most serious consequence of genital herpes, and - is acquired during birth.

Aseptic meningitis.

genital herpes simplex in males genital herpes simplex in females
Genital Herpes Simplex in Males

Genital Herpes Simplex in Females

laboratory diagnosis

Laboratory Diagnosis:

Identification is very important to prevent neonatal infection and HSV encephalitis.

1- Isolation of virus on tissue culture

2- Detection of HSV in vesicle fluid by electron microscopy

3- Detection of viral DNA by PCR

4- Detection of viral antigen by direct immunofluroescence or ELIZA

5- Serological diagnosis to detect IgM antibodies that indicates recent infection or reactivation

diagnosis of hsv 2

Diagnosis of HSV-2:

CytopathicEffect of HSV in cell culture: Positive immunofluorescence test

Note the ballooning of cells. for HSV antigen in epithelial cell.

human cytomegalovirus hcmv

Human Cytomegalovirus (HCMV):

Belong to the betaherpesvirus subfamily of herpesviruses

The name “cytomegalo-” account for the swollen state of virus-infected cells. The infected cells are typically enlarged and multinucleated.

Double stranded DNA enveloped virus

The structure of the genome of CMV is similar to other herpesviruses, consisting of long and short segments which may be orientated in either direction, giving a total of 4 isomers.

A large number of proteins are encoded for, the precise number is unknown.




Sexual intercourse.

Blood transfusion.

Organ transplantation.

Breast feeding.


Primary infection: usually asymptomatic

In symptomatic cases, CMV replicates in epithelial cells of respiratory and gastrointestinal tracts viremia

infection of all organs of the body.

Latency: in monocytes and macrophages.

Reactivation: common in immunocompromised persons.

clinical features

Clinical Features:

Congenital infection: may result in “cytomegalic inclusion disease” leads to congenital abnormalities as:- Growth retardation. - Microcephaly. Hepatosplenomegaly - Thrombocytopenia Blindness

Postnatal infection: usually asymptomatic. However, in a minority of cases, the syndrome of infectious mononucleosis may develop which consists of fever, lymphadenopathy, and splenomegaly.

Infections of immunocompromised patients: such as transplant recipients and AIDS patients are prone to severe CMV disease such as pneumonitis, retinitis, colitis, and encephalopathy.

congenital cytomegalovirus disease

Congenital Cytomegalovirus Disease:

Three-week-old infant with congenital cytomegalovirus infection with purpuricskin lesions andhepatosplenomegaly.

laboratory diagnosis1

Laboratory Diagnosis:

Isolation of the virus from throat washings or urine on tissue culture.

Detection of viral DNA by PCR.

Detection of viral antigens in urine or saliva.

Serodiagnosis: Detection of CMV specific IgM or rising titre of IgG by ELIZA or latex agglutination assay.

Lung section showingtypical owl-eye inclusions

human papillomavirus hpv

Human Papillomavirus (HPV):


Non enveloped, icosahedral, epitheliotropicdouble stranded supercoiled DNA virus.

It is estimated that 75% of the adult population will have at least one HPV infection during their lifetime.

Has great tissue and cell specificity, infecting only surface epithelia of skin and mucous membranes.

The genome is contained within a spherical protein capsid with 7 early proteins (E1 to E7), and 2 late structural proteins (L1 and L2).


Based on L1 gene sequence difference, there are over 100 types of HPV; 40 can cause anogenital infection.

Low-risk HPV types: cause anogenital warts and other benign lesions

High-risk HPV types: are associated with malignant carcinomas (mainly of the cervix).




Sexual contact.

Contaminated surfaces (fomites)

From mother to an infant during delivery (rare)

How Does HPV “Cause” Cancer?

HPV produces a chronic infection of basal cell layer of stratified squamous epithelium.

HPV DNA persist non integrated in normal infected cells.

But integrated in host cell chromosome in high grade dysplasia cells high expression of E6 and E7 genes high expression of E6 and E7 proteins.

hpv infection outcomes

HPV Infection Outcomes

In high-risk HPV strains:

E6 and E7 interact with many cellular proteins, which influence the outcome of infection.

Protein E6 interacts with p53in the host cell and promotes it’s degradation.

Protein E7 complexes withretinioblastomaprotein (Rb), thereby inactivating it.

Rband p53 are both tumor suppressors, involved in DNA repair and cell death.

clinical picture

Clinical Picture:

Genital warts:

- Skin growths in the anogenitalarea with cauliflower-like growths.

- In women, genital warts can appear on the vulva, urethra, cervix, vagina, anus or thighs.

- In men, warts can appear on the penis, scrotum, anus or thighs.

- Genital and anal warts are very contagious.

- Sometimes genital warts last for years and sometimes disappear without treatment..

- Genital and anal warts can sometimes come back.

hpv perianal wart hpv penile warts
HPV Perianal Wart:

HPV Penile Warts:

2 cancer of the genital tissues

2) Cancer of the genital tissues:

High risk types of the HPV virus are linked to cervical cancer as well as cancers of the penis, of the anus and other genital cancers.

In women, pre-cancerous cells can be detected in the cervix by a Pap test.

It is unlikely that a young girl will be diagnosed with cervical cancer as it takes many years for a cancer to develop.

What is a Pap test ?

A Pap test is an examination of a woman’s internal genital organs.

It is the only way to detect abnormal cells in the cervix that could potentially develop into cancer later in life.

A girl should have her first Pap test within 3 years of becoming sexually active.

laboratory diagnosis2

Laboratory Diagnosis:

HPV cannot be cultivated to diagnose infections.

For cervical screening:Cervical swabs or biopsy samples are subjected to:

a. Cytology (Pap smear)

b. Detection of cervical biomarkers: include E6 and E7

c. Hybridization or PCR molecular assays: to detect HPV L1 DNA sequences, E6 or E7 mRNA