Viruses cause diseases in humans, animals and other organisms through a multi-step process that involves invading host cells, reproducing within those cells, and subsequently causing cell damage or death.
- Entry into the Host
For a virus to cause disease, it must first gain entry into the host body through various routes, such as inhalation, ingestion, inoculation through breaks in the skin or mucous membranes, or sexual transmission. Once inside the body, viruses encounter various barriers, including the skin, mucous membranes, and immune defenses, which they must evade or overcome to establish infection.
- Attachment and Entry into Host Cells
Once inside the host, the virus must attach to specific receptors on the surface of susceptible host cells. These receptors are typically proteins or carbohydrates that the virus recognizes and binds to. The specificity of this interaction often determines the tropism of the virus, meaning which types of cells or tissues it can infect. This depends on factors such as receptor availability and cellular permissiveness.
After attachment, the virus enters the host cell. This can occur through various mechanisms, such as fusion with the cell membrane or being engulfed by the cell in a process called endocytosis.
- Replication and Assembly
Once inside the host cell, the virus releases its genetic material (either DNA or RNA) and takes over the cell’s machinery to replicate its own genetic material and produce viral proteins. The host cell’s resources such as enzymes and ribosome are redirected to produce new virus particles instead of normal cellular components.
Newly synthesized viral components are assembled into complete virus particles within the host cell. This assembly may occur in the cytoplasm, nucleus, or at specific cellular membranes, depending on the virus.
- Release of New Viruses
Newly formed viruses are released from the host cell either through cell lysis (the cell bursts open/rupture, releasing viruses) or budding (the virus exits the cell by acquiring a portion of the cell membrane with it as their own envelope in the process).
- Spread and Dissemination: Following primary replication, viruses may spread locally within tissues or disseminate throughout the body via the bloodstream or lymphatic system. This dissemination allows viruses to infect multiple organs and tissues, leading to systemic illness in some cases.
Mechanisms of viral infection and pathogenesis
Viruses can have diverse effects on host cells, ranging from mild alterations in cellular function to cell death and tissue damage. Here are some of the main effects viruses can have on host cells:
- Cellular Damage and Death: Many viruses directly damage or destroy infected host cells as part of their replication cycle. This can occur through various mechanisms, including disruption of cellular membranes, alteration of cellular metabolism, inhibition of cellular protein synthesis, induction of apoptosis (programmed cell death), or direct lysis of the cell membrane to release newly formed virus particles. Cell death can lead to tissue damage and contribute to the pathogenesis of viral diseases.
- Cytopathic Effects: Some viruses induce specific changes in infected host cells known as cytopathic effects (CPEs). These effects can include cell rounding, syncytium formation (fusion of multiple cells), formation of inclusion bodies (dense aggregates of viral proteins or nucleic acids), vacuolization (formation of intracellular vacuoles), or formation of multinucleated giant cells. CPEs can disrupt cellular function and contribute to tissue pathology.
- Immune Activation and Inflammation: Viral infection triggers immune responses in the host, including activation of innate and adaptive immune mechanisms. This immune activation aims to control viral replication and clear the infection but can also contribute to tissue inflammation and damage. Immune cells release cytokines, chemokines, and other inflammatory mediators in response to viral infection, leading to recruitment of immune cells to the site of infection and amplification of the immune response.
- Oncogenesis: Some viruses have oncogenic potential, meaning they can induce cellular transformation and contribute to the development of cancer. These oncogenic viruses may integrate their genetic material into the host cell genome, disrupt cellular regulatory pathways, or promote uncontrolled cell growth and proliferation. Examples of oncogenic viruses include human papillomavirus (HPV), Epstein-Barr virus (EBV), hepatitis B virus (HBV), hepatitis C virus (HCV), and human T-cell leukemia virus (HTLV).
- Persistent Infection and Latency: Certain viruses can establish persistent or latent infections in host cells, where viral replication continues at low levels over an extended period. Persistent viral infections can lead to chronic inflammation, tissue damage, and long-term health consequences. Latent viral infections involve the establishment of viral genomes within host cells without active viral replication, with periodic reactivation leading to recurrent episodes of viral replication and disease.
- Cellular Transformation and Immortalization: Some viruses, particularly certain oncoviruses, have the ability to transform infected host cells, leading to immortalization and malignant transformation. This process involves the activation of oncogenes, inactivation of tumor suppressor genes, and dysregulation of cellular signaling pathways, ultimately resulting in the formation of cancerous cells.