Pathogenesis is simply defined as the mechanism of disease development in a host. The interaction of pathogenic viruses (inclusive of DNA and RNA containing viruses) with host molecules that result in the production of infection or disease is known as viral pathogenesis. Virulence is simply defined as the degree or intensity of the pathogenicity of a given pathogenic microorganism. It is the ability of a microbe (in this case, a pathogenic virus) to invade a host and produce or cause disease or infection. Virulence is a combination of the infectivity and pathogenicity of a pathogenic organism. The virulence of a pathogenic virus depends on the strain of the given virus that invades the host. Two strains of a given virus in the same viral family may vary in their virulence even though they are both pathogenic to the host. Thus, the viral strain that produces a more severe form of the disease is more virulent than the strain that produces a benign disease or infection.

A highly virulent strain of a pathogenic virus causes severe clinical symptoms of the disease than a less virulent strain of the same virus – which usually produce relatively less severe symptoms. The virulence of a virus is different from its infectivity. The infectivity of a pathogenic virus is the ability of the virus to invade a host and establish itself within the cells or tissues of the invaded host. And infectivity is a prerequisite to the development of disease (i.e. viral pathogenesis) within a given host. While some viral infections are subclinical or covert in nature, others are overt ­– and produces clinical signs and symptoms of the disease that they cause. Subclinical viral infections are those viral infections that produce little or no apparent clinical signs and symptoms in the affected host; and they can also be known as inapparent viral infections. Most viral infections are inapparent in nature, and thus they are self-limiting and are countered by the host immune system as aforementioned. In such scenarios, there may be infection without the appearance of clinical illness (i.e. asymptomatic infection), and the host may be exposed to the pathogenic virus without the development of infection or disease.

However, death and severe clinical symptoms may occur in certain viral infections caused by virulent strains of the virus – as is the case for some mutant forms of influenza virus and coronaviruses. Viral infections can also be chronic, acute or latent in occurrence. Chronic viral infections refer to those viral infections that last for a very long time in a host, and they can also be called persistent viral infections. In chronic or persistent viral infections, there is usually a continuous viral replication going on within the host but in a slow progressive manner; and chronic viral infections can be experienced during the latency stage of infection as aforementioned. Chronic viral infections are characterized by the prolonged survival of the invading viral pathogen within the host even long after the host immune system is actually expected to clear the virus from the body. In chronic/persistent viral infections, there is usually little or no appearance of clinical signs and symptoms of the viral disease in the affected host.

Hepatitis B virus (HBV), rubella virus, measles virus, and cytomegalovirus (CMV) are some examples of viral pathogens that establish chronic/persistent viral infections in humans. Acute viral infections are characterized by the rapid onset of disease development; and there is apparent production of clinical signs and symptoms associated with the viral disease in the affected host. It is usually the first stage of viral infections; and most acute infections are normally cleared or warded-off by the immune system of the affected host. Examples of human pathogenic viruses that show acute infection include adenoviruses, influenza viruses and respiratory synctial viruses (RSV) amongst other viral pathogens that attack the respiratory tract of humans and animals. In latent viral infections, there is usually a slow but progressive development of viral infection or disease development in the affected host.

Latent viral infections are infections in which the invading pathogenic virus assumes a covert form, and only produces clinical signs and symptoms of the disease when the viral pathogen becomes reactivated to do so – especially when the host’s immune system is compromised or suppressed. Herpes simplex viruses and varicella-zoster viruses (VZV) are typical examples of some human viruses that assume a latent stage of viral infection. In summary, it should be noted that the steps involved in viral pathogenesis is as the same steps involved in the replication of a virus within a living host as aforementioned. Prior to the development of disease within the host, the pathogenic virus must first gain entry to into the host’s body (viral entry), and thus initiate a primary replication once it has entered a suitable host. Viral entry and cell penetration is vital to the disease development of viral infections.

Pathogenic viruses exhibit cell/tissue tropism – in which a given virus shows affinity to specific host cells or tissues after entry. Tropism is defined as the movement of a pathogenic virus to specific cells or tissues of the host’s body in which they replicate. And it is an important process in viral pathogenesis that occurs immediately after viral entry. For example, Rabies virus that causes rabies in humans has tropism for the nerve cells of the body – which is why the disease (rabies) is characterized by muscular impairment and paralysis in human or animal hosts affected by the virus. After tropism, there is usually the development of clinical features of the disease caused by the invading viral pathogen. And this development is usually countered by the host’s immune system in individuals whose immune system is still intact. However, immunocompromised hosts and those whose immune system is suppressed by chemotherapy or a debilitating disease usually show severe forms of the disease.

There is usually viral shedding during the disease process; and it is at this stage (i.e. viral shedding) that new infectious virions of the invading pathogenic virus are produced. The shedding of infectious viral particles into the environment either through the blood, saliva or feaces marks the last stage of viral pathogenesis. During viral shedding, infected individuals are highly infectious and they could serve as routes via which the pathogenic virus can pass on from an infected individual to a susceptible and non-infected host. Viral shedding allows pathogenic viruses to be maintained within a given population so that the disease they cause can be perpetuated over some certain period of time until a time when sustainable containment and preventive measures are instituted to break the spread and transmission of the disease or disease agents amongst susceptible hosts.

Some pathogenic viruses such as the rabies virus that causes rabies are not actually perpetuated within the population and from an infected individual to a non-infected individual. This is because rabies virus can only infect humans from animals. In other words, animals are the main reservoirs of rabies virus, and humans become infected with the agent when they come in contact with the body fluids of infected animals including dog, fox and wolfs. Humans bitten by such animals can also transmit the virus to their victims. The saliva of such animals is a typical body fluid through which the rabies virus can be transmitted within a defined human population. Thus, there is no viral shedding for rabies infection in humans because humans are the dead end host for such viruses.

Humans infected with rabies virus that fails to recover from the disease eventually die from the infection. Pathogenic viruses affect different parts of the human body including the respiratory tract, gastrointestinal tract, the unborn foetus, the skin and the central nervous systems amongst others; and the progression of the disease varies from one pathogenic virus to another. The good news is that some viral infections are self-limiting and often subsides even without formal treatment. However, antiviral drugs and vaccines are available for the treatment and prevention of human viral infections; and vaccine and drug development is also underway for those viral infections or disease without potent antiviral drugs and vaccines.


Acheson N.H (2011). Fundamentals of Molecular Virology. Second edition. John Wiley and Sons Limited, West Sussex, United Kingdom.

Alan J. Cann (2005). Principles of Molecular Virology. 4th edition. Elsevier Academic Press,   Burlington, MA, USA.

Alberts B, Bray D, Johnson A, Lewis J, Raff M, Roberts K and Walter P (1998). Essential Cell Biology: An Introduction to the Molecular Biology of the Cell. Third edition. Garland Publishing Inc., New York.

Balows A, Hausler W, Herrmann K.L, Isenberg H.D and Shadomy H.J (1991). Manual of clinical microbiology. 5th ed. American Society of Microbiology Press, USA.

Barrett   J.T (1998).  Microbiology and Immunology Concepts.  Philadelphia,   PA: Lippincott-Raven Publishers. USA.

Leave a Reply

Your email address will not be published. Required fields are marked *