Impact of Viruses for Human Life

The study of viruses has historically provided and continues to provide the basis for much of our most fundamental understanding of modern biology, genetics, and medicine. Virology has had an impact on the study of biological macromolecules, processes of cellular gene expression, mechanisms for generating genetic diversity, processes involved in the control of cell growth and development, aspects of molecular evolution, the mechanism of disease and response of the host to it, and the spread of disease in populations.

In essence, viruses are collections of genetic information directed toward one end: their own replication. They are the ultimate and prototypical example of “selfish genes.” The viral genome contains the “blueprints” for virus replication enciphered in the genetic code, and must be decoded by the molecular machinery of the cell that it infects to gain this end. Viruses are, thus, obligate intracellular parasites dependent on the metabolic and genetic functions of living cells.

Submicroscopic, different viruses range in size from smaller than the smallest organelle to just smaller than the simplest cells capable of energy metabolism and protein synthesis, the mycoplasma and simple unicellular algae. Despite their diminutive size, they have evolved and appropriated a means of propagation and replication that ensures their survival in free-living organisms that are between 10 and 10,000,000 times their size and genetic complexity.


The effect of virus infections on the host organism and populations — viral pathogenesis, virulence, and epidemiology 

The replication and propagation of a given virus in a population is frequently (but not always) manifest with the occurrence of an infectious disease that spreads between individuals. The study of effects of viral infection on the host is broadly defined as the study of viral pathogenesis. The sum total of the virus-encoded functions that contribute to virus propagation in the infected cell, in the host organism, and in the population is defined as pathogenicity of the given virus. This term essentially describes the genetic ability of members of a given specific virus population (which can be considered to be genetically more or less equivalent) to cause a disease and spread through (propagate in) a population. Thus, a major factor in the pathogenicity of a given virus is its genetic makeup or genotype.

The basis for severity of the symptoms of a viral disease in an organism or a population is complex. It results from an intricate combination of expression of the viral genes controlling pathogenicity, physiological response of the infected individual to these pathogenic determinants, and response of the population to the presence of the virus propagating in it. Taken together, these factors determine or define the virulence of the virus and the disease it causes.

A basic factor contributing to virulence is the interaction among specific viral genes and the genetically encoded defenses of the infected individual. It is important to understand, however, that virulence is also affected by the general health and genetic makeup of the infected population, and in humans, by the societal and economic factors that affect the nature and extent of the response to the infection.

The distinction and gradation of meanings between the terms pathogenesis and virulence can be understood by considering the manifold factors involved in disease severity and spread exhibited in a human population subjected to infection with a disease-causing virus. Consider a virus whose genotype makes it highly efficient in causing a disease, the symptoms of which are important in the spread between individuals—perhaps a respiratory infection with accompanying sneezing, coughing, and so on. This ideal or optimal virus may (and often does) incorporate numerous genetic changes during its replication cycles as it spreads in an individual and in the population. Some viruses generated during the course of a disease may, then, contain genes that are not optimally efficient in causing symptoms. 

Such a virus is of reduced virulence, and in the extreme case, it might be a virus that has accumulated so many mutations in pathogenic genes that it can cause no disease at all (i.e., has mutated to an avirulent or apathogenic strain). While an avirulent virus may not cause a disease, its infection may well lead to complete or partial immunity against the most virulent genotypes in an infected individual. This is the basis of vaccination,. But the capacity to generate an immune response and the resulting generation of herd immunity also means that as a virus infection proceeds in a population, its virulence either must change or the virus must genetically adapt to the changing host.

Other factors not fully correlated with the genetic makeup of a virus also contribute to variations in virulence of a pathogenic genotype. The same virus genotype infecting two immunologically naive individuals (i.e., individuals who have never been exposed to any form of the virus leading to an immune response) can cause very different outcomes. One individual might only have the mildest symptoms because of exposure to a small amount of virus, or infection via a suboptimal route, or a robust set of immune and other defense factors inherent in his or her genetic makeup. Another individual might have a very severe set of symptoms or even death if he or she receives a large inoculum, or has impaired immune defenses, or happens to be physically stressed due to malnutrition or other diseases.

Also, the same virus genotype might cause significantly different levels of disease within two more-or-less genetically equivalent populations that differ in economic and technological resources. This could happen because of differences in the ability of one society’s support net to provide for effective medical treatment, or to provide for isolation of infected individuals, or to have available the most effective treatment protocols.

Taken in whole, the study of human infectious disease caused by viruses and other pathogens defines the field of epidemiology (in animals it is termed epizoology). This field requires a good understanding of the nature of the disease under study and the types of medical and other remedies available to treat it and counter its spread, and some appreciation for the dynamics and particular nuances and peculiarities of the society or population in which the disease occurs. 

The interaction between viruses and their hosts 

The interaction between viruses (and other infectious agents) and their hosts is a dynamic one. As effective physiological responses to infectious disease have evolved in the organism and (more recently) have developed societally through application of biomedical research, viruses themselves respond by exploiting their naturally occurring genetic variation to accumulate and select mutations to become wholly or partially resistant to these responses. Such resistance has led to periodic or episodic reemergence of diseases thought to have been controlled. 

The accelerating rate of human exploitation of the physical environment and the accelerating increase in agricultural populations afford some viruses new opportunities to “break out” and spread both old and novel diseases. Evidence of this is the ongoing acquired immune deficiency syndrome (AIDS) epidemic, as well as sporadic occurrences of viral diseases, such as hemorrhagic fevers in Asia, Africa, and southwestern United States. Investigation of the course of a viral disease, as well as societal responses to it, provides a ready means to study the role of social policies and social behavior of disease in general. 

The recent worldwide spread of AIDS is an excellent example of the role played by economic factors and other aspects of human behavior in the origin of a disease. The causative agent, human immunodeficiency virus (HIV), may well have been introduced into the human population by an event fostered by agricultural encroachment of animal habitats in equatorial Africa. This is an example of how economic need has accentuated risk. 

HIV is not an efficient pathogen; it requires direct inoculation of infected blood or body fluids for spread. In the Euro-American world, the urban concentration of homosexual males with sexual habits favoring a high risk for venereal disease had a major role in spreading HIV and resulting AIDS throughout the male homosexual community. A partial overlap of this population with intravenous drug users and participants in the commercial sex industry resulted in spread of the virus and disease to other portions of urban populations. The result is that in Western Europe and North America, AIDS has been a double-edged sword threatening two disparate urban populations: the relatively affluent homosexual community and the impoverished heterosexual world of drug abusers—both highly concentrated urban populations. In the latter population, the use of commercial sex as a way of obtaining money resulted in further spread to other heterosexual communities, especially those of young, single men and women. 

An additional factor is that the relatively solid medical and financial resources of a large subset of the “economic first world” resulted in wide use of whole blood transfusion, and more significantly, pooled blood fractions for therapeutic use. This led to the sudden appearance of AIDS in hemophiliacs and sporadically in recipients of massive transfusions due to intensive surgery. Luckily, the incidence of disease in these last risk populations has been reduced owing to effective measures for screening blood products. 

Different societal factors resulted in a different distribution of HIV and AIDS in equatorial Africa and Southeast Asia. In these areas of the world, the disease is almost exclusively found in heterosexual populations and much more frequently in women than in men. This distribution of AIDS occurred because a relatively small concentration of urban commercial sex workers acted as the source of infection of working men living apart from their families. The periodic travel by men to their isolated village homes resulted in the virus being found with increasing frequency in isolated family units. Further spread resulted from infected women leaving brothels and prostitution to return to their villages to take up family life. 

(Meyda Azzahra)