Initial Stages of Pathogenesis
The entry portal for the infection is most frequently the upper respiratory tract. In complicated cases, the pathogen can immediately invade the lower respiratory tract and affect the alveoli. This leads to the development of primary acute viral pneumonia, which is one of the leading causes of mortality in high-risk patient groups.
At the cellular level, the pathological process unfolds in several stages:
- Replication: The virus actively multiplies within the epithelial cells of the respiratory tract.
- Host Response: As a nonspecific antiviral defense mechanism, infected cells begin to synthesize interferon.
- Morphological Changes: Inflammation and edema rapidly increase in the tissues. The basement membrane swells, and the superficial epithelial layer undergoes desquamation (shedding).
- Consequence: The epithelial barrier is disrupted, providing a pathway for the virus to spread further throughout the body.
Pathogenetic Mechanisms of Injury
After overcoming local defense barriers, systemic mechanisms of tissue injury are triggered, which determine the severity of the disease:
- Toxic and Sensitizing Effects. The primary cause of systemic toxicity is not only the pathogen itself, but also the breakdown products of the patient's own destroyed cells, which are actively absorbed into the systemic circulation.
- Vascular Bed Injury. The pathogen can activate the proteolytic system. This leads to direct damage of the capillary endothelium and a sharp increase in the permeability of vascular walls and serous membranes. In clinical practice, this mechanism manifests as hemorrhages, severe hemodynamic disturbances, and microcirculatory disorders.
- Impact on the Immune System. The infection induces a transient secondary immunodeficiency. Temporary depression of host defenses creates ideal conditions for secondary bacterial superinfection.
Clinical Presentation and Periodization
The course of the disease can be divided into three key periods: incubation (lasting 1–2 days), period of clinical manifestations (3 to 7 days), and convalescence (recovery takes 7–10 days).
Influenza A has the most severe clinical course, characterized by the following syndromes:
- Intoxication Syndrome: Onset is always acute, accompanied by severe chills, high fever, cephalalgia, myalgia, and arthralgia.
- Respiratory Syndrome: Pronounced upper respiratory catarrh develops. Patients experience rhinitis, dysphonia, substernal chest pain, and a characteristic dry, hacking cough.
- Neurotropism: Influenza A virus is capable of invading the nervous system. There is a high risk of neurotoxicosis, which is particularly dangerous in pediatric practice and can be fatal.
- Hemorrhagic Syndrome: Due to vascular damage, there is increased bleeding tendency, with potential hemorrhages into the skin, mucous membranes, and parenchymatous organs.
- Abdominal Syndrome: Occurs relatively rarely, predominantly in children. It manifests as abdominal pain and dyspeptic disorders.
Complications and Features of Other Viral Types
Infections complications pose a direct threat to the patient's life and are divided into three main groups:
- Specific: Caused directly by the virus itself (e.g., hemorrhagic pneumonia or pulmonary edema).
- Bacterial: Superinfection secondary to immunodeficiency. Most commonly caused by S. pneumoniae or S. aureus.
- Organ-specific: Severe systemic impairment of central nervous system, hepatic, renal, and cardiovascular functions.
Unlike influenza A, influenza B presents with a significantly milder clinical course. It completely lacks neurotropism, but features a specific clinical trait: a propensity for ocular involvement (developing conjunctivitis and photophobia). Influenza C is characterized by the mildest course among all variants.
Immune Response
The body's fight against the infection proceeds in stages, engaging various arms of the immune system:
- Early Phase (During Acute Illness): Innate immune factors react first. Massive production of $\alpha$-interferon is triggered. Local immunity in the respiratory tract is established via secretory IgA.
- Humoral Response: Synthesis of strain-specific virus-neutralizing antibodies begins. Their blood concentration peaks 2–3 weeks after disease onset.
- Cellular Response (During Convalescence): NK cells (natural killers) and specific cytotoxic T lymphocytes are activated to completely clear the pathogen from the body.
Post-infection immunity is long-lasting and robust, but it is highly specific—protection works exclusively against the specific viral variant that caused the disease.