Overview of Viral Infections

7th lecture of Medical Virology for 3rd Year Students

Presented by Dr. Mohammed J. M. Shallal
Overview of Viral infections





Viruses gain access to the human body primarily inhaling aerosolized droplets from coughing or sneezing. Also occur by touching the nose or mouth by hand or other object exposed to the virus. Despite the normal host protective mechanisms which are including
The mucous covering most surfaces,
Ciliary action,
Collections of lymphoid cells,
Alveolar macrophages,
Secretory IgA.

Many viral infections remain localized in the respiratory tract, although some viruses produce systemic spread (eg, chickenpox, measles, rubella).
Overview of Acute Viral Respiratory Infections


The symptoms depend on whether the infection is concentrated in the upper or lower respiratory tract.

Definitive diagnosis requires:

1) Isolation of the virus
2) Identification of viral gene sequences
3) Demonstration of a rise in the antibody titer

the specific viral disease can frequently be deduced by considering the major symptoms, the patient's age, the time of year, and any pattern of illness in the population.

The severity can range from inapparent to overwhelming.

The most severe illness is usually seen in infants (paramyxoviruses) and in elderly or chronically ill adults (influenza virus).





A few viral agents, such as herpes simplex virus and Epstein-Barr virus, probably infect cells in the mouth.

In the intestinal tract it exposed to harsh elements (acid, bile salts, and proteolytic enzymes).


Consequently, viruses are all acid- and bile salts-resistant.

There may also be virus-specific secretory IgA and nonspecific inhibitors of viral replication to overcome.

Overview of Viral Infections of the GIT

Acute gastroenteritis is with symptoms ranging from mild, watery diarrhea to severe febrile illness characterized by vomiting, diarrhea, and prostration.

Rotaviruses, Norwalk viruses, and caliciviruses are major causes of gastroenteritis. Infants and children are affected most often.

Some enteric viruses utilize host proteases to facilitate infection (proteolytic digestion of viral capsid that then facilitates events such as virus attachment or membrane fusion).

Enteroviruses, coronaviruses, and adenoviruses gastrointestinal infections are often asymptomatic.

Some enteroviruses (polioviruses, and hepatitis A virus) are important causes of systemic disease but do not produce intestinal symptoms.

The skin is a tough and impermeable barrier to the entry of viruses.

However, a few viruses are able to breach this barrier and initiate infection of the host through:

• Small abrasions of the skin (poxviruses, papilloma-viruses, herpes simplex viruses)

• The bite of arthropod vectors (arboviruses)
• Infected vertebrate hosts (rabies virus, herpes B virus)
• Injected during blood transfusions or via contaminated needles, such as acupuncture and tattooing (hepatitis B virus, HIV).


Overview of Viral Skin Infections

Some viral agents produce localized lesions (papillomaviruses and molluscum contagiosum). But most viruses are spreading to other sites.

The epidermal layer is devoid of blood vessels and nerve fibers, so viruses that infect epidermal cells tend to stay localized.

Viruses introduced deeper into the dermis reach blood vessels, lymphatics, dendritic cells, and macrophages and usually spread and cause systemic infections.

Such viral infections originate by another route (eg, measles virus) infections occur via the respiratory tract), and the skin becomes infected from below.

Lesions in skin rashes are designated as macules, papules, vesicles, or pustules.

Macules which are caused by local dilation of dermal blood vessels.

Papules occurs if edema and cellular infiltration present in the area.

Vesicles occur if the epidermis is involved, and they become pustules if an inflammatory reaction delivers polymorpho-nuclear leukocytes to the lesion.

Ulceration and scabbing follow. Hemorrhagic and petechial rashes occur when there is more severe involvement of the dermal vessels.

Vesicles

Infectious virus is not shed from the maculopapular rash of measles or from rashes associated with arbovirus infections.

In contrast, skin lesions are important in the spread of poxviruses and herpes simplex viruses

(high titers in the fluid of these vesiculo-pustular rashes, and they are able to initiate infection by direct contact with other hosts).

Overview of Viral Infections of the CNS

Viral infection of CNS is always a serious matter.

Viruses can gain access to the brain by two routes:

• 1) by the bloodstream (hematogenous spread)
• 2) by peripheral nerve fibers (neuronal spread).
* blood spreading may occur by:
• through endothelium of small cerebral vessels.
• passive transport across the vascular endothelium.
• through the choroid plexus to the cerebrospinal fluid.
• transport within infected monocytes, leukocytes, or lymphocytes.
Once the blood-brain barrier is breached, more extensive spread throughout the brain and spinal cord is possible.


* Spreading of virus via peripheral nerves.

Virions can be taken up at sensory nerve or motor endings and be moved within axons, through endoneural spaces, or by Schwann cell infections.

Herpes viruses travel in axons to be delivered to dorsal root ganglia neurons.

The virus may utilize more than one routes of spread.

Many viruses, including herpes-, toga-, flavi-, entero-, rhabdo-, paramyxo-, and bunyaviruses, can infect the central nervous system and cause meningitis, encephalitis, or both.

Encephalitis caused by herpes simplex virus is the most common cause of sporadic encephalitis in humans.

Pathologic reactions to cytocidal viral infections of the central nervous system include necrosis, inflammation, and phagocytosis by glial cells.

The post-infectious encephalitis (after measles infections and after rubella infections) is characterized by demyelination without neuronal degeneration and is probably an autoimmune disease.

The neurodegenerative disorders, called slow virus infections, are uniformly fatal.

Features of these infections include a long incubation period (months to years) followed by the onset of clinical illness and progressive deterioration, resulting in death in weeks to months; usually only the central nervous system is involved.

Some slow virus infections, such as progressive multifocal leuko-encephalopathy JC (John Cunningham) polyomavirus) and subacute sclerosing panencephalitis (measles virus), are caused by typical viruses.


Overview of Congenital Viral Infections

Viral diseases produce in the human fetus.

Most maternal viral infections do not result in viremia and fetal involvement. if so, serious damage may be done to the fetus.

Three principals involved in the production of congenital defects are:

(1) the ability of the virus to infect the pregnant woman and be transmitted to the fetus;
(2) the stage of gestation at which infection occurs;
(3) the ability of the virus to cause damage to the fetus directly, or indirectly, by infection of the mother resulting in an altered fetal environment (eg, fever).

The sequence of events that may occur prior to and following viral invasion of the fetus

21
Primary viral agents responsible for congenital defects (Rubella virus and cytomegalovirus).

Or can occur by (herpes simplex, varicella-zoster, hepatitis B, measles, and mumps virus and with HIV, parvovirus, and some enteroviruses)

In utero infections may result (fetal death, premature birth, intrauterine growth retardation, or persistent postnatal infection).

Developmental malformations (congenital heart defects, cataracts, deafness, microcephaly, and limb hypoplasia. Fetal tissue is rapidly proliferating.


Viral infection and multiplication may destroy cells or alter cell function.

Lytic viruses, such as herpes simplex, may result in fetal death.

Less cytolytic viruses, such as rubella, may slow the rate of cell division.

If this occurs during a critical phase in organ development, structural defects and congenital anomalies may result.

Viral infections may be transmitted from the mother to fetus:

* During delivery (natal) from contaminated genital secretions, stool, or blood.

* Less commonly, viral infections may be acquired during the first few weeks after birth (postnatal) from maternal sources, family members, hospital personnel, or blood transfusions.

Host age is an important factor in virus pathogenicity.

More severe viral diseases is often presented in newborns.

* In addition to development of the immune response with age.

* There seem to be age-related changes in the susceptibility of certain cell types to viral infection.


Viral infections usually can occur in all age groups but may have their major impact at specific times of life.

Examples include rubella, which is most serious during gestation; rotavirus, which is most serious for infants; and St. Louis encephalitis, which is most serious in the elderly.
Effect of Host Age

Thank you