Herpes Simplex Virus

Alferez, Donna Gabrielle Ann A.

Introduction
It is a viral disease from the herpesviridae family Involves the mucocutaneous surfaces, the CNS and visceral organs Oral herpes is the most common

Etiology
Genome: linear, double stranded DNA molecule that encodes >90 transcription units with 84 identified proteins. In a regular icosahedral protein shell which is composed of 162 capsomeres.

After the fusion and entry of the viral envelope and the cell membrane, the nucleocapsids > cytoplasm Others turn on the transcription of early genes of HSV replication.

Etiology
After the replication of the viral genome and the synthesis of structural proteins, nucleocapsids are assembled in the nucleus of the cell.

Two types of inclusion bodies:

Type A Basophilic Feulgen-positive bodies which contains viral DNA Eosinophilic inclusion bodies that are devoid of the viral nucleic acid or protein and represent a scar of viral infection

Etiology
Does not result in the cells death. Viral genomes are maintained by the cell in a repressed state compatible with survival and normal activities of the cell > Latency
Latency is associated with the transcription of only a limited number of virus encoded proteins.

Etiology
With the release of the HSV from the neuron and its subsequent entry into the epithelial cells result in viral replication, the destruction of the cells, and the subsequent reappearance of virus on the mucosal surface. > Reactivation

Pathogenesis
Exposure at the mucosal surfaces are abraded skin sites permit entry of the virus and initiation of its replication Initial phase of the infection, viral replication occurs in the ganglia and contiguous neural tissue.

Pathogenesis
Spreads to the other mucocutaneous surfaces through centrifugal migration of infectious virions via the peripheral sensory nerves.

Immunity
Immunocompromised patients with defects in the cell-mediated immunity experience more severe and more extensive HSV infections. Multiple cell population, including natural killer cells, macrophages and a variety of T lymphocytes play a role in host defenses against HSV infections Lymphokines generated by T lymphocytes.

Epidemiology
HSV 1 is acquired more and earlier than HSV 2 >90% of the adults have anitibodies to HSV 1 by the fifth decade of life Low socioeconomic status > most persons acquire HSV 1 infection before they reach their third decade of life

Epidemiology
Antibodies to HSV 2 cannot be detected until puberty Correlate with past sexual activity and vary great among populations

HSV 2 has decreased over the past 5 years in the US

Epidemiology
High prevalence of HSV 2 in Central America, South America and Africa Many cases of asymptomatic genital HSV 2 infection are unrecognized Shown pictures of genital lesions, >60% subsequently identify episodes of symptomatic reactivation

Epidemiology
High rates of mucocutaneous reacticvation suggest that exposure to HSV from sexual or other close contact is common and help explain the spread and high prevalence of HSV infection worldwide.

Transmission
Easily transmitted by direct contact with a lesion or the body fluid of an infected individual. Skin-to-skin contact during periods of asymptomatic shedding. Contact with persons who have active ulcerative lesions or those with no clinical manifestations of the infection Exposure to HSV through sexual contact or any other forms of close contact

Oral Facial Infections

Visible sores or ulcers. Early stages of orofacial herpes and genital herpes are harder to diagnose; laboratory testing is usually required Gingivostomatis and pharyngitis are the most common clinical manifestation of the first episode of HSV 1 infection.

 Herpes labialis is the most common clinical manifestation of reactivation of HSV 1 infection Result from primary infection and are usually seen in children and young adults. Signs and symptoms : fever, malaise, myalgias, inability to eat, irritability and cervical adenopathy which can last 3-14 days

 Extend into the mucosal and deep cutaneous layers. Friability, necrosis, bleeding, severe pain and inability to eat or drink may result Persistent ulcerative HSV infection are among the most common infections in patients with AIDS Systemic antiviral therapy speeds the rate of healing and relieves the pain of mucosal HSV infections in immunosuppressed patients.

Genital infections
First episode > fever, headache, malaise and myalgias. Pain, itching, dysuria, vaginal and urethral discharge and tender inguinal lymphadenopathy are the predominant local symptoms Cervix and the urethra

HSV vaginal tract disease is manifested by endometritis and salpingitis in women and prostatitis in men.

Herpetic Willow
The finger; Complication of primary oral or genital herpes by inoculation of virus through a break in the epidermal surface or by direct introduction of virus into the hand through occupational or some other type of exposure Signs and symptoms: edema, erythema and localized tenderness Antiviral chemotherapy

Herpes Gladiatorum
Any area of the skin Mucocutaneous HSV infections of the thorax, ears, face and hands Common in wrestlers

Eye infections
Common cause of corneal blindness in the US Acute onset of pain, blurred vision, chemosis, conjunctivitis and dedritic lesions of the cornea.

Central and Peripheral nervous system infections

Accounts for 10-20% of all cases of sporadic viral encephalitis in the US Most adults with encephalitis have clinical or serologic evidence of mucocutaneous HSV 1 infection before the onset of CNS symptoms

Antiviral chemotherapy with acyclovir reduces the rate of death from HSV encephalitis

Visceral infections
Result from viremia and multiple organ involvement is common Clinical manifestations involve only the esophagus, lung or liver HSV esophagitis may result from direct extension of oral pharyngeal HSV infection into the esophagus

 HSV pneumonitis is uncommon except in severely immunosuppressed patients and may result from extension of herpetic tracheobronchitis into lung parenchyma Complications: monarticular arthritis, adrenal necrosis, idiopathic thrombocytopenia and glomerulonephritis

 Occasionally disseminates to other visceral organs such as the adrenal glands, pancreas, small and large intestines and bone marrow In pregnant women associated with the death of both the mother and the fetus.

Neonatal HSV infections

<6 weeks have the highest frequency of visceral or CNS infections Skin lesions do not develop All neonates with presumed neonatal herpes should be treated with IV acyclovir

Antiviral chemotherapy with a high dose of IV acyclovir has reduced the mortality rate from neonatal herpes

Diagnosis
Confirmed in the laboratory by detection of the virus or viral DNA in scrapings from the lesions Antiviral therapy with valacyclovir has been shown to reduce the transmission of HSV 2 between sexual partners.

Prevention
Contraception Consistent use is effective in reducing the risk of genital HSV 2 transmission

Medical Management
Many aspect of mucocutaneous and visceral HSV infections are amenable to anitiviral chemotherapy For mucocutaneous infections, acyclovir, famciclovir and valacyclovir have been mainstays in the therapy

Acyclovir is frequently used and is available in IV, oral, topical formulations

 Famciclovir, an oral formulation of penciclovir is effective in treatment for HSV 1 and HSV 2 infections Shorten the duration of the symptoms and lesions of mucocutaneous HSV infections Recent studies show that high dose short course oral therapy is effective in reducing signs and symptoms of both oral and genital infection

OT Management
Group therapy Arts and Crafts