Classification by the result of interaction with the cell
Depending on whether the pathogen successfully completes the replication cycle, three main types of interaction are distinguished:
- Productive infection. Proceeds in permissive (susceptible) cells. The virus unimpeded goes through a complete replication cycle, which successfully ends with the formation of new infectious progeny.
- Abortive infection. Characterized by the interruption of the cycle at one of the stages—new full-fledged viral particles are not formed. This can happen due to the genetic non-permissiveness of the cell itself (absence of necessary factors or presence of blocking mechanisms). Another reason is infection with defective viruses that lack a complete set of genes for replication (like hepatitis D virus, which requires the presence of hepatitis B virus). Also, the process can be interrupted by defective interfering particles (DI particles), which compete with homologous complete viruses. They weaken the lethal effect of the pathogen, but contribute to 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. At the same time, even cytolytic viruses under such conditions may not destroy the cell, but only alter its activity (for example, disrupt cholesterol and hormone synthesis) or trigger tumor transformation.
Interaction of genomes and outcome for the cell
According to how viral and cellular genetic material interact, two variants are distinguished:
- Autonomous infection: the viral nucleic acid replicates completely independently of the host chromosomes.
- Integrative infection (virogeny): the genetic code of the pathogen is integrated into the cell DNA and copied along with it. Clinically, this mechanism is extremely important, as it is often what triggers the development of chronic and autoimmune diseases.
According to the outcome for the infected cell, infections are divided into:
- Cytolytic: end in 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. At the same time, viruses are capable of altering the functional activity of the cell or causing its malignant transformation without changing morphology immediately.
Infection often activates apoptosis—programmed cell death. This is a natural defense mechanism of the body that prevents the pathogen from spreading. In response to this, some agents (e.g., poxviruses) have acquired genes encoding specific anti-apoptotic proteins during evolution.
Spread of the virus at the macroorganism 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 pathways 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 areas.
- Neural — progression along nerve trunks.
- Hematogenous — the most frequent pathway, in which dissemination occurs via the bloodstream.
It is the hematogenous pathway that often leads to the phenomenon of secondary localization (clearly manifested in poliomyelitis). First, the virus multiplies at the entry portal, forming a primary focus (small intestine epithelium). If the body's resistance is overcome, viremia occurs—the release of the pathogen into the blood. Next, the virus reaches the target organs (in this case, CNS structures), forming a secondary focus, which is clinically manifested by the development of paralysis.
According to the scale of damage at the organism level, focal infections (action limited to the site of the entry portal) and generalized infections (pathogen spreads through the body with the formation of multiple secondary foci) are distinguished.
Briefly: answers to topical questions
Which viruses are capable of causing integrative infection (virogeny)?
Integrative infection (virogeny) can be caused by:
- Temperate DNA-containing bacteriophages.
- Oncogenic viruses.
- Certain infectious DNA-containing viruses — for example, hepatitis B virus.
- Certain infectious RNA-containing viruses — for example, HIV.
Which viruses synthesize specific anti-apoptotic proteins?
Specific anti-apoptotic proteins are encoded by certain viruses, such as poxviruses. Infection can trigger apoptosis as a defense reaction of the body, and some viruses have genes encoding anti-apoptotic proteins.
Which viruses use the neural pathway of dissemination in the body?
The neural pathway of dissemination is used by the rabies virus (RABV). This neurotropic virus penetrates the network of neurons of the peripheral nervous system, where its primary multiplication occurs. Then new virions undergo centripetal retrograde axonal transport, reaching the neurons of the spinal cord and brain. After accumulation in CNS structures, the virus spreads centrifugally along efferent fibers of peripheral nerves to various organs and tissues, primarily the salivary glands and cornea.
What mechanisms of viral entry into a susceptible cell exist?
Viral entry into a susceptible cell is carried out by several active mechanisms depending on the structure of the virion:
- Fusion of the virion with the cell membrane — characteristic of enveloped viruses (herpesviruses, retroviruses). Specific fusion proteins integrate the lipoprotein envelope of the virus into the cell membrane, releasing the internal component into the cytosol.
- Receptor-mediated endocytosis (viropexis) — characteristic of non-enveloped viruses (adenoviruses). The virus is captured by the membrane and internalized within an endosome.
- Pore formation (direct translocation) — the capsid protein forms a channel in the membrane through which viral RNA is injected into the cytoplasm (poliovirus).
- Macropinocytosis — penetration via the formation of a large fluid-filled vacuole.
The pathways of viral spread in the body are easy to remember by their initial letters (abbreviation H-S-C-S-N): Hematogenous, Secretory, Contact, Syncytial, Neural.
Class and exam questions
What is an abortive infection and why does it occur?
This is a type of infection in which the virus replication cycle is interrupted and new infectious particles are not formed. The causes may include the absence of necessary factors within the cell itself (non-permissiveness), infection with a defective virus lacking a full set of genes, or exposure to defective interfering particles.
What is the difference between cytolytic and non-cytolytic infection?
Cytolytic infection inevitably leads to destruction (lysis) and death of the infected cell. In the non-cytolytic variant, the cell remains viable, continues to perform its functions, and simultaneously releases new viral particles.
Why do viruses need anti-apoptotic proteins?
The body uses apoptosis (programmed death of the infected cell) as a defense reaction to stop pathogen replication. Inhibitor proteins synthesized by certain viruses (e.g., poxviruses) block this process, allowing the virus to complete its replication cycle.
How are secondary foci of viral infection formed?
After primary replication at the entry site, the virus can enter the systemic circulation (viremia). Via the bloodstream, it reaches target organs sensitive to it (e.g., nervous tissue in poliomyelitis), where it settles and causes the formation of a secondary pathological focus.
What else to study on this topic
- Acute and persistent infections: classification by duration
- The role of defective interfering particles in the formation of persistent infection
- Tumor transformation of cells in restrictive and non-cytolytic interaction
- The phenomenon of extreme parasitism: dependence of hepatitis D virus on hepatitis B
- Clinical significance of integrative infection (virogeny) in the development of autoimmune diseases
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