Homoeopathic approach in herpes simplex virus

Dr Shantipriya

ABSTRACT
Herpes simplex virus type 1 and type 2 (HSV-1 and HSV-2, respectively), Herpes simplex virus (HSV) is indeed a ubiquitous, enveloped, double-stranded DNA virus. It cause a variety of diseases, including cold sores, genital herpes, herpes stromal keratitis, meningitis and encephalitis ,etc . Homeopathic medicines are often explored for their potential roles in treating and preventing various infectious conditions, including herpes simplex virus infection.

KEY WORDS: Herpes simplex virus, Transmission, Pathophysiology , complication, Homeopathy Medicine.

INTRODUCTION
Herpes has been known for at least 2000 years, In the United States 16.2% of people, aged 14 to 49 years have genital herpes simplex virus-2 (HSV-2) infection. Many people infected with HSV-2 display no physical symptoms and are described as asymptomatic or having sub-clinical herpes. Herpes virus infections primarily include infections caused by HSV-1 and HSV-2, these viruses are also known as human herpes virus 1 and 2 (HHV-1 and HHV-2). These viruses belong to the family of herpes viridae. Both HSV-1 and HSV-2 are ubiquitous and contagious. They can spread when an infected person is producing and shedding the virus by inoculation, kissing and sexual intercourse.

HERPIS SIMPLEX VIRUS
Virus consists of a large double stranded, linear (DNA) genome. Encased within an icosahedral protein cage called capsid, which is wrapped in a lipid bilayer called the envelope. This complete particle is known as the virion. Both HSV1 and HSV-2 contain at least 74 genes.

TRANSMISSION
HSV-1 and HSV-2 are transmitted both horizontally and vertically. Horizontal transmission occurs during close contact with an infected person who is shedding virus from the skin, often in saliva or in secretion from the genitals. Transmission is most likely when sores are present, through viral shedding and transmission can occur in the absence of visible sores and most HSV-2 infection results from asymptomatic shedding.HSV-2 is primarily a sexually transmitted disease whereas HSV-1 is usually acquired orally during childhood. Both viruses may be transmitted from mother-to-child before or during child birth.

The risk of the infection is highest if the mother becomes infected at around the time of delivery (transmission risk 30% to 60%); the risk fall to 3% if it is a recurrent infection and is less than 1% if there are no visible lesions. Entry of HSV into the host cell involves interaction of several glycoproteins on the surface of the enveloped virus, with receptors on the surface of the host cell After binding the virus fuses with the host cell membrane and creates an opening or pore through which the virus enters the host cell. From the cellular cytoplasm, viral capsid enters the cell nucleus by creating a nuclear entry pore. HSV evades the immune system through interference with MHC class I presentation of antigen on the cell surface.

PATHOPHYSIOLOGY
Exposure to HSV at mucosal surfaces or abraded skin sites permits entry of the virus and initiation of its replication in cells of the epidermis and dermis. Initial HSV infection is often subclinical, without apparent lesions. In animal models and human subjects, both clinical acquisition and subclinical acquisition are associated with sufficient viral replication to permit infection of either sensory or autonomic nerve endings. After transversing the neuroepithelial gap and entering the neuronal cell, the virus or, more likely the nucleocapsid is transported intra-axonally to the nerve call bodies in ganglia. For HSV1 infection, trigeminal ganglia are most commonly infected, although extension to the inferior and superior cervical ganglia also occurs. For HSV2 infection, sacral nerve root ganglia are most commonly affected. Viral replication occurs in ganglia and contagious neural tissue during primary infection only. After initial inoculation of neural ganglion, virus spread to other mucosal skin surfaces by centrifugal migration of infectious virions through peripheral sensory nerves. This mode of spread explains the characteristics development of new lesions distant from initial crop of vesicles in patients with primary genital or orofacial HSV infection, the large surface area over which these vesicles may be visualized, and recovery of virus from neural tissue distant from neurons innervating the inoculation. Contagious spread of virus may also takes place via autoinoculation and allow further extension of disease.

Viremia is present approximately 25% of primary HSV2 infections, and its presence may affect the natural history of HSV2 disease in terms of site, severity and frequency of reactivation. Recent studies suggest that reactivation is far more frequent and dynamic than previously recognized. Clinical studies demonstrate that host factors also influence a reactivation. Immunocompromised patients have more severe disease. Antibodies that develop following an initial infection with type of HSV prevents reinfection with type same virus type – a person with history of orofacial infection caused by HSV1 cannot contract herpes whitlow or genital infection caused by HSV1.If an oral HSV1 infection is contracted first, seroconversion will have occurred after 6 weeks to provide protective antibodies against a future HSV1 infection,

CLINICAL MANIFESTATIONS
Lesions may appear anywhere on the skin or mucosa, but are most frequent around or in the mouth or on the lips, conjunctiva, cornea, and genitalia. After a prodromal period of tangling discomfort or itching, the clusters of small, tense vesicles appear on an erythematous base. Clusters vary in size from 0.5 to1.5 cm but may coalesce. Lesions on nose, ears, eyes, fingers or genitalia may be particularly painful. Vesicles typically persist for a few days, then rupture and dry forming a thin yellowish crust. Healing generally occur 8 to 12 days after the onset. Lesions usually heel completely but recurrent lesions at the same site may cause atrophy and scarring. Skin lesions can develop secondary bacterial infection. Localised infections can disseminate in immunocompromised patients.

Herpes Labialis :

It usually occurs as a secondary outbreak of HSV.  It develops as ulcers (cold sores) on the vermilion border of the lip. Acute Herpetic Gingivostomatitis :This usually results from primary infection with HSV-1, typically in children. Occasionally through oral-genital contact, the HSV-2 can also lead to gingivostomatitis. Intra-oral and gingival vesicles rupture, usually within several hours to 1 or 2 days. Fever and pain are often present, at times there may be difficultly in eating and drinking.

Herpetic Whitlow:

It is a painful swollen lesion of the distal phalanx of finger or thumb. It results from inoculation of HSV through the skin and is most common among health care workers. Occasionally infection occurs on the toes or on the nail cuticle.

Herpes Gladiatorum:

Individuals that participate in contact sports, such as wrestling, rugby, or soccer, sometimes acquire this condition caused by HSV-1. It presents as skin ulceration on face, ears and neck, accompanied by fever, headache, sore throat and swollen glands. It occasionally affects the eyes or eyelids

Genital Herpes :

Genital herpes is the most common ulcerative STD in the developed countries. It is usually caused by HSV-2 although 10% to 30% of cases involve HSV-1. Genital HSV-2 is more common in women. The vesicles usually erode to form ulcer that may coalesce. Lesions may occur on prepuce, glans penis and penile shafts in men and on the labia, clitoris, vagina, perineum and cervix in women. These may occur around the anus and in the rectum in men or women who engage in receptive anal intercourse

Genital HSV infection may cause urinary hesitancy, dysuria, urinary infection in counterparts. In some cases severe sacral neuralgia may occur. Scarring may follow healing and re-currences occur in 80% with HSV-2 and in 50% with HSV-1 cases. Primary genital lesions are usually more painful, prolonged and widespread and are more likely to be bilateral and involve regional lymphadenopathy and constitutional symptoms than recurrent genital lesions. Recurrent lesions may have severe prodromal symptoms and may involve the buttocks, groin or thigh.Some individuals with HSV-2 infection never have sores, or they may have very mild sign that they do not even notice. People diagnosed with a first episode of genital herpes can expect to have several (typically four or five) symptomatic recurrences within a year.

Over the time these recurrences usually decrease in frequency.

Herpetic Keratoconjunctivitis :

Primary infection typically presents as swelling of the conjunctiva and eyelids (blepharoconjunctivitis). Infection of the corneal epithelium causes pain, tears, photophobia and corneal ulcers, that often have a branching pattern

HSV Encephalitis :

It is the commonest form of sporadic viral encephalitis. Cases are seen throughout the year and the age distribution is biphasic with peaks at 5 to 30 years and above 50 years of age. HSV-1 causes more than 95% of cases of HSV encephalitis. The pathogenesis of HSV encephalitis varies.

In children and young adults, the primary HSV infection may result in encephalitis, presumably exogenously. Acquired virus enters the CNS by neurotropic spread from the periphery via olfactory bulb.Most of the adults with HSV encephalitis have clinical or serological evidence of HSV1 infection prior to onset of CNS symptoms.

Patient may present with headache, seizures, confusion, stupor or coma.Late manifestations include olfactory or gustatory hallucinations, anosmia, temporal lobe seizures, aphasia, hemiparesis and abnormalities in behaviour.Rarely an affliction of memory may be present, but this becomes evident only later in the convalescent states of illness, as a patient awakens from stupor or coma.

Swelling and herniation of one or both temporal lobes through tentorium may occur, leading to Deep coma and respiratory arrest during the first three days.

Herpes Viral Meningitis:

HSV-2 is the most common cause of Mollaret’s meningitis, a type of recurrent viral meningitis. Besides the above-mentioned disorders, HSV has been associated with various neuronal disorders, like Bell’s palsy and Alzheimer’s disease.The presence of HSV-1/DNA in saliva at a higher frequency in patients with Bell’s palsy relative to those without the condition, has supported that reactivation of latent HSV-1 inside the geniculate ganglia may cause it. In the presence of certain gene variation (APOE-epsilon 4 carriers), HSV-1 increases one’s risk of developing Alzheimer’s disease.

DIAGNOSTIC TESTS:

• Detecting Viral Glycoproteins
• Western Blot Assay:
• Detecting Viral Genetic Material

1)Polymerase Chain Reaction

2)Loop-Mediated Isothermal Amplification Technique

3)Helicase-Dependent Amplification Technique

• Detection of Viral Antibodies in Blood
• Passive Agglutination or Hemagglutination
• Enzyme-Linked Immunosorbent
• Fluorescence Immunoassay
• Multiplexed Flow Immunoassay
• Luciferase Immunoprecipitation Assay
• Microfluidic-Based Point-of-Care Devices

COMPLICATIONS

1)Neurological complications:

Although HSV-1 has a predilection for the development of encephalitis after intracerebral injection in the mouse model, HSV-2 generally causes meningitis. However, the meninges are not the only component of the CNS involved in HSV-2 infection. Virtually any part of the neuraxis may be affected by this virus, including the retina, brain, brainstem, cranial nerves, spinal cord, and nerve roots.

2)Neonatal herpes simplex encephalitis:

When HSV-2 infection is mentioned, neonatal herpes simplex encephalitis (HSE), a devastating disorder, is the disease most commonly considered.Seventy percent of affected neonates are born to mothers without symptoms or signs of genital herpes. Recent studies suggest that as much as 30% of neonatal HSE is due to HSV-1. The risk of acquisition during a primary infection with HSV-1 or HSV-2 is 50%.Risk factors for neonatal HSV disease include first-episode maternal infection in the third trimester, invasive monitoring, delivery before a gestational age of 38 weeks, and maternal age of less than 21 years.Delivery by cesarean section significantly reduces the risk of HSV acquisition. In mothers who are seropositive for HSV-2 only, the risk to the neonate is less than 1%.Dissemination to the CNS occurs in 70% of all infected neonates and is most commonly heralded by the appearance of focal or generalized seizures. Skin lesions are observed in 66%.

3)Acute aseptic meningitis in adults:

Aseptic meningitis occurs in 36% of women with primary HSV-2 genital infection and 13% of menAseptic meningitis is a rare manifestation of primary HSV-1 genital infection and a rare complication of recurrent genital infections due to HSV-1 and HSV-2.During the prodrome of genital herpes and concomitant with the herpetic eruption, affected patients experience headache, neck stiffness, and low-grade fever. Back, buttock, perineal, and lower extremity pain may be associated with urinary retention and constipation

4)Hsv-2 ascending myelitis:

Thoracic or lumbosacral ascending myelitis is also seen with HSV-2 infection but almost exclusively in immunocompromised patients, particularly those with HIV infection. The lesions may be necrotizing and, if so, have a poor prognosis. Recurrent disease also has been described.The clinical presentation is characterized by pain, often anogenital or radicular, with associated limb numbness, paresthesias, and weakness. Herpetic skin lesions may accompany the neurological manifestations.

5)Hsv-2 radiculopathy:

In autopsy studies, 40% of sacral dorsal root ganglia contain dormant HSV-2. Only 5% of these individuals had recognized genital herpes infection during life.Obtaining a history of recurrent genital herpes outbreaks occurring contemporaneously with the radicular symptoms is very helpful diagnostically. Radiculopathy caused by HSV-2 infection typically affects the lumbar or sacral nerve roots and is often recurrent. In addition to radicular pain, paresthesias, urinary retention, constipation, anogenital discomfort, and leg weakness may be observed.

6)Acute retinal necrosis:

Acute retinal necrosis is heralded by red eye, periorbital pain, and impaired visual acuity. Examination results will show episcleritis or scleritis, keratic precipitates, retinal vasculitis, and necrosis with retinal detachment.

Typically, this sight-threatening disorder has a bimodal age distribution, with varicella zoster virus and HSV-1 infections affecting older patients and HSV-2 infection affecting patients with a median age of 20 years. Acute retinal necrosis may occur in association with HSV-2.

PREVENTION

• Sexual abstinence is the only method for absolute prevention of genital herpes.
• Contact should be avoided when active lesions are present. Avoid contact until re-epithelialization has occurred.
• Use of condoms and spermicidal foams is recommended in patients who have a history of recurrent herpes genitalis.

HOMEOPATHIC MANAGEMENT:

VACCININUM

• Vaccine poison is capable of setting up a morbid state of extreme chronicity, named by Burnett Vaccinosis, symptoms like those of Hahnemann’s Sycosis.
• Neuralgias, inveterate skin eruptions, chilliness, indigestion with great flatulent distension (Clark).
• Hot and dry.
• Pimples and blotches.
• Eruption like variola.

MERCURIUS SOLUBILIS

• Almost constantly moist.
• Persistent dryness of the skin contra indicates mercurius.
• Excessive odorous viscid perspiration; worse, night.
• General tendency to free perspiration, but patient is not relieved thereby.
• Vesicular and pustular eruptions.
• Ulcers, irregular in shape, edges undefined.
• Pimples around the main eruption.
• Itching, worse from warmth of bed.
• Crusta lactea; yellowish-brown crusts, considerable suppuration.

RHUS TOXICODENDRON

• Red, swollen; itching intense.
• Eye painful on turning it or pressing, can hardly move it, as in acute retrobulbar neuritis. – Profuse gush of hot, scalding tears upon opening lids.Swelling of glands and prepuce-dark-red erysipelatous; scrotum thick, swollen, oedenatous. Itching intense.Swelling, with intense itching of vulva.
• Pelvic articulations stiff when beginning to move. – Adynamic; restless, trembling. –

GRAPHITES

• Tendency to skin affections and constipation, fat, chilly, and costive, Rough, hard, persistent dryness of portions of skin unaffected by eczema.
• Eruptions, oozing out a sticky exudation.
• Rawness in bends of limbs, groins, neck, behind ears.
• Unhealthy skin; every little injury suppurates.
• Ulcers discharging a glutinous fluid, thin and sticky.
• Phlegmonous erysipelas of face; burning and stinging pain.
• Eruption of red spots, one inch in diameter, little elevated, but having milky, bluish-white vesicles, apparently papillary, one line in diameter, and not very high; constantly tormented by violent itching and burning; felt as if she must tear it with her nails, but only rubbed it, followed by such an aggravation that she wept; face warm and flushed; menses late, having been checked near end of last period by getting feet wet.
• Herpes exuding a sticky matter.
• Circular herpes feels hard to touch and wrinkled, situated in bend of left elbow, which itched terribly.

NATRIUM MURIATICUM

• Miliary eruption, with shooting pain.
• Itching and pricking in skin.
• Rash over whole body, with stinging sensation skin.
• Pain and redness of an old cicatrix.
• Skin of hands, esp. about nails, dry, cracked; hang-nails.
• Whitish hives on arms and hands.
• Itching tubercles.
• Nettle-rash after violent exercise (itching).
• Exanthema on mouth; lips; in intermittent fever where there are large exanthematous spots looking like large peas, on lips (cold sores); lips look puffy.

SULPHUR

• Itching, burning; worse scratching and washing.
• Troubles of very long standing resulting from suppressed eruptions.
• Skin dry; rough; scaly; voluptuous itching – “feels so good to scratch”; ecchymosis.
• Itching in skin, even of whole body, agg. at night, or in morning, in bed, and often with pain as of excoriation, heat, itching (soreness), or bleeding of the part which has been scratched.
• Eruptions, like those which often follow vaccination.
• Herpetic, red, irregular, furfuraceous spots, or covered with small phlyctenae, discharging a serous lymph.
• Scabious eruptions.
• Burning itching of the eruptions.
• Hepatic spots of a yellow or brownish colour (on the body).
• Erysipelatous inflammation, with pulsative and shooting pains.
• Bright scarlet redness over whole body.
• Tingling in the skin throughout the body.
• The skin cracks easily, esp. in open air; cracks, with pain, as from excoriation.

PHYTOLACCA

• Itches, becomes dry, shrunken, pale.
• Papular and pustular lesions.
• Most useful in early stages of cutaneous diseases.
• Disposition to boils, and when sloughing occurs.
• Squamous eruptions.
• Syphilitic eruptions.
• Venereal buboes.
• Scarlatina-like rash.Skin cool, shrivelled, dry, lead-colored.
• Barber’s itch (local application of tincture).
• Itch (a salve made from the roots), old cases where Sulphur did no good.
• Salt rheum and itch.
• Squamous eruptions, pityriasis;
• A very ugly, black-looking, tettery eruption, communicated from one person to others (decoction from roots).
• Scarlatina; high fever, headache, both sides of throat covered with membrane, with rash .

APIS MELLIFICA  

• Swelling and dry erysipelatous redness.
• Rash disappears suddenly, leaving scattered red spots or points.- Eruption receding, short of breath, sleepless, restless, scanty urine, great thirst, or none at all.  Confluent variola.
• Eruption upon inner thighs, below knees, upon hands, face, back of neck, still more on central portions of body; small pustules, with burning, smarting, stinging, forming dry scabs of laminated form, scaly, brownish, sometimes light straw color.
• Small pustules arose under skin, with burning, smarting and stinging; when ripe, small scales on them, dry, brownish, or straw-colored; on inside of thighs, under knees, or hands, in face or neck, most towards middle of body; tincture in water. – ¤ Hard, red, somewhat conical swellings, occurring usually on lower limbs, below knees, sometimes on arms, rarely on other parts of body, varying in number and size, from a half dime to an inch or two in diamete

RANUNCULUS BULBOSUS

• Frequent and violent itching in different parts of skin.
• Lancinations in skin, which change to itching.
• Vesicular eruptions, like blisters after a burn.
• Deep blue vesicles, small, deep, transparent, thickly grouped, with burning itching and hard and tettery scabs. –  vesicles filled with serum which burn, may have a bluish-black appearance; especially when following course of supraorbital or intercostal nerves and followed by sharp stitching pains.
• Herpes : preceding neuralgia costalis; on fingers and in palm of hand; over whole body.

  MEZEREUM

• Dry, burning, itching herpetic eruption on both hands and left foot; skin peeled off.
• Nocturnal itching on arms, legs, back, amel by scratching, but immediately returning on some other place.
• Red itching rash on arms, head and over whole body.
• Violent itching rash on nape of neck, back and thighs, always agg and gnawing after scratching and sticking as from needles.
• Itchlike eruption, after vaccination, depriving child of sleep.
• Herpes, with severe neuralgic pains, itching after scratching turns into burning, agg in bed, from touch; vesicles form brownish scab.
• Neuralgia and burning after zona.
• Vesicles appear around ulcers, itching violently and burning like fire; after eight days these vesicles dry up, leaving scabs, the tearing off of which causes great pain and retards healing.
• Whole skin covered with elevated white scabs.
• Moist, scabby eruption.
• Crusty eruptions, white scabs, bleeding when touched.
• Vesicular erysipelas.
• Vesicles appear around ulcers, itch violently, burn like fire; fiery red areola, shining like fire.

PHOSPHORUS

• Exanthema which comes out in pustules; is scaly.
• Wounds which appear to have healed break out again and bleed; wounds that continually heal and break out again.
• Desquamation of skin.
• Burning in the skin.
• Tingling in skin.

 SEPIA OFFICINALIS

• Herpes circinatus in isolated spots.
• Itching, stinging, lancinating, burning, or sometimes indolent ulcers (knuckles, finger-joints, tips of fingers, joints and tip of toes).
• Hepatic spots.Herpetic eruption on lips and about mouth.
• Red herpetic spots on both sides of neck with much itching.
• Reddish herpetic spots above hips.
• Lentil-sized brown spots on elbows, surrounded with a herpetic-looking skin.
• Fine rash over body, particularly about bends of elbows and knees; prickling, tingling and itching; in a warm room it remained out and she felt well, if she passed into a cold room it disappeared and she had the most severe rheumatic pains in and about these joints.
• Moist pimply eruption at margin of vermilion border of upper lip.
• Herpes circinatus.

CONCLUSION
To effectively manage and treatment HSV-1 and HSV-2, it is important to focus on both preventing recurrence and minimizing the severity of outbreaks. There is a requirement for successful treatment that prevents or minimizes the recurrence of HSV-1 and HSV-2 episodes and further decreases the severity of exacerbations. In homeopathy, treatments have been clinically proven to have some impact, and solutions for herpes viruses. Homeopathy can prevent further outbreaks of herpes simplex infection. Homeopathic remedies which can be used for herpes infection are Natrum Mur,  Sulph, Graphites, Phosphorus , Sepia officinalis , Mezereum, Rhus tox,  Phytolacca, Apis,  Ranunculus bulbosus   etc

REFERENCES

1. William Boericke’s New Manual of Homoeopathic Materia Medica with Repertory. Revised and augmented 3e: B Jain Publishers, New Delhi.
2. Clarke J H. A Dictionary of Practical Materia Medica. Jain Publishers, New Delhi.
3. API Text book of medicine
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5. HERING C., Guiding Symptoms of our Materia Medica (hr1)
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7. Berger JR, Houff S. Neurological complications of herpes simplex virus type 2 infection. Arch Neurol. 2008;65(5):596-600. doi:10.1001/archneur.65.5.596
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Dr Shantipriya
PG scholar, Department of Practice of Medicine
Government Homoeopathic Medical College and Hospital Bangaluru, 560079
Shantipriya13101996@gmail.com

Under the Guidance of:
Dr  Mahabubali Nadaf
Assistant professor, Department of Practice of Medicine
Government Homoeopathic Medical College and Hospital,Bangaluru, 560079