ARTICLE ON VIRAL INFECTIONS

 BY SUNNDEEP CHOPRA:

Viruses normally comprise of a nucleic acid surrounded or engulfed by one or more proteins. Some viruses also have or are then fortified with an outer membrane (jelly like) envelope. A predominant majority of viruses are obligate intracellular parasites who can only replicate, recreate, procreate, multiply within cells as their nucleic acids do not encode or ingest the many enzymes essential or necessary for protein, carbohydrate or then lipid metabolism and for the generation or creation of high-energy phosphates.

Viral nucleic acids typically engulf or ingest proteins essential for replicating or recreating/repackaging their nucleic acids within the biochemical milieu or folds of host cells.

Viral infection is initiated or heralded by adsorption (is the adhesion of atoms, ions, biomolecules, or then molecules of gas, liquid or dissolved solids to a surface) of the virus to the cells’ surface. Adsorption is normally a by-product or then follows on from the molecular interaction of viral surface proteins with receptors on the cells’ plasma membrane.

Viruses penetrate or permeate the cell membrane by fusing or aligning with it after adsorption. The resultant reaction hastens the process behind the virus’s partial decomposition or degeneration. The virus as a result becomes insensitive to neutralizing anti bodies as it penetrates, permeates and enters the cytoplasm.

Penetration and uncoating or extricating result in or cause/result in viral nucleocapsid or then  nucleoprotein entry into the cytoplasm.

SYMPTOMS: The first or primary episode or manifestation of viral infection can last for a period ranging between a few measly days to a few long drawn out weeks. The concentration or then multiplication of viruses at the host site/infection site constantly vacillates or then rises and plummets usually to immeasurable or non-registerable/recordable levels.

The rate of intensity or virility of the viral infection is codependent on the accessibility or availability of a particular organ or tissue to both the virus as well as systemic immune effectors, the intrinsic or inherent ability of the virus to replicate or multiply at the host site and absence of endogenous, nonspecific as well as specific resistance.

Infections caused by or then intimately linked with the enterovirus, mumps virus, measles virus, rubella virus, rotavirus, influenza virus, AAV, adenovirus, HSV and VZV are cleared or then banished from the host sites within a matter of three-four weeks. A few of these viruses are extremely proficient in or then past masters at altering/changing, evading or then escaping from the clutches of both the innate and acquired immune responses of the host cells or organisms thereby ensuring the months long longevity  of cytomegalovirus infections.

Disease infestations or manifestations can be directly attributed to the viral replication and consequent inflammatory response at the host site but are not inextricably interlinked with the levels of replication or manifestation at that site.

Primary or commonplace infections are more often than not cleared or cured by non-specific, innate and specific adaptive immune responses.

PERSISTENT AND LATENT INFECTIONS: A miniscule minority of the vast conglomeration of viruses possess the wherewithal to cause or then give rise to either persistent or latent infections; with the rabies, measles and HIV viruses being notable exceptions to the afore mentioned rule.

DNA viruses or life cell viruses as they have come to be called commonly are normally known to have significantly lower mutation (permanent change in the DNA sequence of a gene) rates. Their persistence or then longevity within the human race or population is mostly attributed to their inherent ability to establish or then cause latent ( a lingering or continual infection that may continue to lie dormant within the host organism or body for an indeterminant period of time) infections and reactivate or rejuvenate themselves from the same.

PERSISTENT VIRAL INFECTIONS AND CANCER: Persistent or lingering viral infection is estimated (supposed) to be the root or then primary cause of/behind as much as/many as 20% of all recorded human malignancies. Cancer is normally a purely accidental, coincidental and extremely are long term effect or manifestation of infections allied with cancer causing cells (oncogenic human viruses).

A viral infection is a highly critical and significantly determinant initial or early step in such malignancies. The same usually or then almost always succeeds in/ or then is successful in it’s evil intentions of forcing or coercing infected cells to enter or permeate the cell cycle thereby considerably enhancing their rate and chances of survival.

A unusual nay freakish virus-infected cell undergoes or then progresses through the subsequent genetic changes that permit or then create congenial conditions for the enhanced or significantly increased autonomous or then completely free from any encumberance growth and survival rate or characteristic of a malignant or disease bearing cell.

VIRAL INFECTIONS:

Family and Representative Viruses:

RNA Viruses:

A.      Picornaviridae: polio virus, coxsackie virus, echovirus, enterovirus, rhinovirus, hepatitis A virus.

B.      Caliciviridae: Norwalk agent, hepatitis E virus.

C.      Togaviridae: rubella virus, eastern equine encephalitis virus, western equine encephalitis virus.

D.     Flaviviridae: yellow fever virus, dengue virus, saint Louis encephalitis virus, west nile virus, hepatitis C virus, hepatitis G virus.

E.      Coronaviridae: coronaviruses.

F.       Rhabdoviridae: rabies virus, vesicular stomatitis virus.

G.     Filoviridae: Marburg virus, ebola virus.

H.     Paramyxoviridae: parainfluenza virus, respiratory synctial virus, Newcastle disease virus, mumps virus, rubeola (measles) virus.

I.        Orthomyxoviridae: Influenza A, B and C viruses.

J.        Bunyaviridae: hantavirus, California encephalitis virus, sandfly fever virus

K.      Arenaviridae: lymphocytic chorioemningitis virus, lassa fever virus, south American hemorrhagic fever virus.

L.       Reoviridae: rotavirus, reovirus, Colorado tick fever virus.

M.   Retroviridae: Human T-lymphotropic virus types I and II, Human immunodeficiency virus types 1 and 2.

DNA Viruses:

Ø  Hepadnaviridae: Hepatitis B virus.

Ø  Parvoviridae: Parvovirus B 19

Ø  Papovaviridae: Human papillomaviruses, JC virus, BK virus.

Ø  Adenoviridae: Human adenoviruses.

Ø  Herpesviridae: Herpes simplex virus types 1 and 2b, Varicella-zoster virus ©, Epstein-Barr virus (d), Cytomegalovirus (e), Human herpesvirus 6, Human herpesvirus 7, Kaposi’s sarcoma-associated herpesvirus (f).

Ø  Poxviridae: variola (smallpox) virus, orf virus, Molluscum contagiosum virus.

FIDELITY OF VIRAL REPLICATION: Hundreds of thousands nay millions of progeny/subsidiary viruses/offshoots/replicas may/can be produced/mutated from a single-virus infected cell. A significant majority of or then many particles partially or incompletely assemble or mutate and thereby never mature or grow into virions. Many mature appearing or then complete looking virions are imperfect and hence possess only incomplete or non-functional genomes.

A typical or then stereotypical virus-infected cell releases or spews out 10-1000 infectious progeny or offshoots despite it’s inherent structure or then formation related flaws. A few of these progeny or offshoots may contain genomes that are significantly different from those who typically infected the cell.

Miniscule, smaller or defective virus genomes have been closely identified with the replication or then recreation of many a RNA and DNA virus/viruses. Virions with defective or then diseased/mutated genomes are inherently capable of being produced in enormously large numbers through packaging of incompletely synthesized or processed nucleic acid.

Adenovirus related or associated packaging or enveloping is grossly or notoriously insufficient , and a high or significant ratio of particle to infectious virus may limit or then impede the amount or numbers of recombitant viruses that can be administered or reused for gene therapy.

VIRAL INFECTION CONTAGIOUS: The capsid (shell of protein that protects the nucleic acid of a virus) and envelope or outer shell/covering of a virus protect its genome or central part and thereby permit or facilitate its efficient transmission from cell to cell and other prospective or likely hosts. Most common and widely prevalent viral infections are either spread through direct contact, by ingestion of contaminated food or water, or then by inhalation of aerolised particles.

The infection normally begins to announce or then manifests itself on an epithelial or mucosal surface and then laterally spreads along it or from it to deeper tissues. The infection subsequently spreads throughout the body like the proverbial wildfire via the bloodstream, lymphatics or then neural circuits.

A few or miniscule minority of viruses are transmitted only amongst humans. The utter or then complete dependence of small pox and polio virus infections on inter human transmission or transfers have enabled health authorities to exterminate the same from amongst humans by resorting to or then taking recourse to mass inoculations or vaccinations.

Certain species of animals too are important or significant reservoirs and vectors of/for transmission of viruses capable of causing human disease. Herpes B, monkeypox, and viral hemorrhagic fevers are prime examples or manifestations of zoonotic infections caused or resulting from either by direct contact with the transmitting animals or then transmission  from animals through other vectors or sources.  

RESISTANCE TO VIRAL INFECTIONS: The initial  or primary resistance or opposition to viral infections is always provided by factors or elements that are not quintessentially virus-specific or related.Physical protection is provided by the multifarious layers or levels of the skin and by the mucous secretions oozing out of the mucal membranes or surfaces.

Interferons (or IFNs- are proteins made and released by host cells in response to the presence of pathogens-such as bacteria, viruses or parasites) are induced or produced and they offer doughty resistance to virus replication or multiplication as soon as the first cell is infected. Viral infections have also been known to trigger or release cytokines (are small or minute cell signaling protein molecules that are secreted by the glial cells present in the nervous system) from infected cells and these cytokines in turn could/may be chemotactic or complementary to inflammatory and immune cells.

Virus specific antibody responses or mechanisms such as virus-specific HLA class II-restricted, CD4+ helper, T lymphocyte responses and virus specific HLA class- I restricted CD8+ cytotoxic T lumphocyte responses or counter measures begin to assert and express themselves within a 7-10 day span after the onset of the infection. These responses whose magnitude or enormity proportionally increases over and through the second and third weeks of the infection discharge a significant role in the recovery of the patient.

DIAGNOSIS: A multitude of methods and techniques are now in vogue as regards the clinical diagnosis of viral infections. Serology (is a blood test that is administered to register the presence of antibodies against a microorganism) and viral isolation or segregation in tissue cultures continue to remain the stereotypical and most prominent methods of diagnosis.

Immunofluorescence, hemadsorption and hemagglutination assays or then tests for antiviral bodies are both labour and time intensive and are hence beginning to make way for enzyme linked immunosorbent assays (ELISAs). ELISAs generally or then almost always use specific viral proteins that are most frequently targeted or then singled out by the anti-body responses. Virus isolation or segregation depends upon the manifestation or occurrence of an infection within susceptible or easily affected cells and the subsequent replication or multiplication in newly infected cells.

Virus growth or progression in cell cultures can often/frequently be identified by its ensuing effects on cell morphology or structure under light microscopy. For example HSV produces or manifests a typical or stereotypical cytopathic effect in a rabbit’s  kidneys within a measly 3 days.   

DRUG TREATMENT FOR VIRAL INFECTIONS: Multiple or multifarious steps in the viral cycle can be effectively targeted or controlled with the initiation of anti-viral drug based treatments. Nucleoside and nonnucleoside reverse transcriptase inhibitors prevent or inhibit synthesis of the HIV provirus, while protease inhibitors block the maturation of the HIV polyprotein after the cell is duly infected.

Virus genomes or manifestations have been known to evolve suitable or appropriate resistance to drugs by either mutation or selection, recombination or renewed alliance with a drug resistant virus, or (in the unique case of the influenza virus and other multicomponent RNA virus genomes) by reassortment or reinvention. The emergence of these species can really prove to be a headache for specialists and medical practitioners as these drug-resistant strains or sub-species can severely limit or inhibit the efficacy or effectiveness of prevalent anti-bacterial drugs.

Excessive and improper or inappropriate usage of anti-viral therapy or drugs can prove to be the foundation stone or then facilitate the emergence of drug-resistant strains as in the case with anti-bacterial therapy. HIV genotyping is a rapid and clinical method in vogue for the identification and splendid isolation of drug-resistant viruses.

PREVENTION: The emergence and subsequent effectiveness of viral vaccines have duly been noted or then accorded pride of place amongst the most accomplished and far reaching advances in medical science. Small pox has been completely eradicated or abolished of the face of this earth except as a potential weapon of biological warfare or bioterrorism.

Experts are extremely enthused about the polio virus following suit. Measles have been almost totally contained and a few strains have also been exterminated. Excess or sizeable mortality and deaths due to or on account of influenza virus epidemics can be effectively prevented and the omnipotent threat of influenza pandemics can be significantly decreased or weeded out by resorting to either contemporary killed or then live attenuated influenza vaccines.

Mumps, Rubella and chickenpox have almost become a relic of the past within the developed countries thanks to the development and widespread administration of childhood vaccines for the same, reimmunisation of adults can be used as an effective tool in controlling the onwards spreading of herpes zoster.

The entry and development of newer and more efficacious varieties of ant virus vaccines does indeed hold out renewed hope about a totally virus free environment in the not too distant future.