Classification by Outcome of Interaction with the Cell
Depending on whether the pathogen successfully completes its replication cycle, three main types of interaction are distinguished:
- Productive infection. Occurs in permissive (susceptible) cells. The virus unimpeded goes through a full replication cycle, which successfully culminates in the formation of new infectious progeny.
- Abortive infection. Characterized by the interruption of the cycle at one of the stages—new complete viral particles are not formed. This can happen due to genetic non-permissiveness of the cell itself (lack of necessary factors or presence of blocking mechanisms). Another reason is infection with defective viruses that lack a full set of genes for replication (such as hepatitis D virus, which requires the presence of hepatitis B virus). The process can also be interrupted by defective interfering particles (DI particles), which compete with homologous complete viruses. They weaken the lethal effect of the pathogen but promote the transition of the disease into a persistent form.
- Restrictive (limited) infection. Occurs when cells are permissive only temporarily. The pathogen persists inside until the functional "maturation" of the cell, or replicates exclusively in a small fraction of the cell population. In this case, even cytolytic viruses under such conditions may not destroy the cell, but merely alter its activity (e.g., disrupt cholesterol and hormone synthesis) or trigger oncogenic transformation.
Genome Interaction and Outcome for the Cell
Based on how viral and cellular genetic material interact, two variants are distinguished:
- Autonomous infection: the viral nucleic acid replicates completely independently of host chromosomes.
- Integrative infection (virogeny): the pathogen's genetic code is integrated into the cell's DNA and copied along with it. Clinically, this mechanism is extremely important as it frequently triggers chronic and autoimmune diseases.
By the outcome for the infected cell, infections are divided into:
- Cytolytic: end in the death and lysis (destruction) of the host cell.
- Non-cytolytic: do not cause immediate lysis. The cell continues to function while simultaneously producing viral particles. Meanwhile, viruses are capable of altering the cell's functional activity or causing its malignant transformation without immediately changing morphology.
Infection frequently activates apoptosis—programmed cell death. This is a natural defensive mechanism of the organism that prevents the pathogen from spreading. In response, some agents (e.g., poxviruses) have evolved genes encoding specific anti-apoptotic proteins.
Spread of the Virus at the Organism Level
The transition of the infectious process from the cellular level to the organ level occurs as a result of the death and disintegration of infected cells. Several routes of further viral dissemination are distinguished:
- Contact — direct transmission to adjacent healthy tissues.
- Syncytial — via intercellular cytoplasmic bridges formed by membrane fusion.
- Secretory — along with mucous membrane secretions to both nearby and distant sites.
- Neural — movement along nerve trunks.
- Hematogenous — the most frequent route, in which dissemination occurs via the bloodstream.
Hematogenous spread frequently leads to the phenomenon of secondary localization (clearly manifested in poliomyelitis). First, the virus multiplies at the portal of entry, forming a primary focus (epithelium of the small intestine). If host resistance is overcome, viremia ensues—the release of the pathogen into the blood. Next, the virus reaches target organs (in this case, CNS structures), forming a secondary focus, which is clinically expressed by the development of paralysis.
According to the scale of damage at the organism level, focal infections (action limited to the site of entry) and generalized infections (pathogen spreads through the body with the formation of multiple secondary foci) are distinguished.