Viruses are obligate intracellular parasites, meaning they can multiply only inside living cells.
When a virus infects a host cell, it can cause a wide range of effects — from no visible damage (latent infection) to cell destruction or transformation into a cancer cell.
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The interaction between a virus and its host cell is therefore central to understanding viral pathogenesis, immunity, and oncogenesis (cancer formation).
2. Stages of Virus–Cell Interaction
- Attachment (Adsorption):
The virus binds to specific receptors on the host cell membrane.
Example: HIV binds to CD4 receptors on T-helper cells. - Penetration:
The virus or its genetic material enters the cell via endocytosis or membrane fusion. - Uncoating:
The viral capsid is removed, releasing the nucleic acid into the cytoplasm. - Replication and Synthesis:
The virus uses host machinery to synthesize its nucleic acids and proteins. - Assembly (Maturation):
Newly synthesized viral components assemble into complete virions. - Release:
Mature viruses exit the cell by lysis (cell destruction) or budding (without immediate cell death).
Each of these stages may alter cellular structure or function, producing the effects of viral infection described below.
3. Effects of Virus Infection on Host Cells
The consequences of viral infection depend on:
- The type of virus
- The host cell type
- The immune response
- The number of infecting virions
A. Cytopathic Effects (CPE)
These are visible morphological and biochemical changes in infected cells, observable under the microscope.
| Type of CPE | Description | Examples of Viruses |
| Cell rounding and detachment | Cells lose shape, detach from the surface | Poliovirus, Adenovirus |
| Cell lysis | Complete destruction of host cells | Enteroviruses |
| Syncytium formation | Fusion of several cells into multinucleated giant cells | Measles virus, RSV, Herpesvirus |
| Inclusion bodies | Aggregates of viral material inside nucleus/cytoplasm | Negri bodies (Rabies), Cowdry A (Herpes), Guarnieri (Poxvirus) |
| Chromosomal damage | Alterations in host DNA | Herpes simplex, Adenovirus |
| Apoptosis (Programmed cell death) | Induced by viral proteins | HIV, Influenza, Hepatitis C |
| Cell transformation (oncogenic) | Conversion to cancerous cells | HPV, Epstein–Barr virus |
B. Physiological and Biochemical Changes
- Inhibition of host DNA, RNA, and protein synthesis
(The virus uses the cell’s machinery for its own replication.) - Alteration of membrane permeability
Causes ion imbalance and cell swelling. - Cytoskeletal disruption
Leads to abnormal cell morphology. - Interference with cell cycle regulation
Some viruses push the cell into continuous division. - Release of lysosomal enzymes
Contributes to cell death.
C. Types of Viral Infections in Cells
| Type of Infection | Description | Example |
| Acute (productive) infection | Rapid viral replication → cell death | Influenza virus |
| Persistent infection | Virus remains in cells for long periods with low-level replication | Hepatitis B, C |
| Latent infection | Virus lies dormant and reactivates under stress | Herpes simplex, Varicella-zoster |
| Transforming infection | Alters cell growth → leads to cancer | HPV, EBV, HTLV |
| Abortive infection | Virus enters but cannot replicate fully | Some defective adenoviruses |
4. Cancer and Viruses (Oncogenic Viruses)
Oncogenic viruses are viruses capable of inducing cancer (tumors) in animals or humans.
They alter the normal regulatory mechanisms of cell growth, causing uncontrolled cell division.
B. Mechanisms of Viral Oncogenesis
- Insertional Mutagenesis (Integration of Viral DNA)
- Viral genome integrates into host DNA and disrupts normal gene regulation.
- Example: Hepatitis B virus (HBV) and Human papillomavirus (HPV).
- Activation of Oncogenes (proto-oncogenes → oncogenes)
- Viral genes activate cellular proto-oncogenes that regulate growth and differentiation.
- Inactivation of Tumor Suppressor Genes
- Viral proteins inactivate tumor suppressor genes such as p53 and Rb.
- Example: HPV E6 and E7 proteins block p53 and Rb.
- Chronic Inflammation and Regeneration
- Long-term viral infection leads to cell damage, inflammation, and increased mutation rate.
- Example: Hepatitis C virus (HCV) → liver cirrhosis → hepatocellular carcinoma.
- Expression of Viral Oncogenes (v-onc genes)
- Some viruses carry their own oncogenes that directly transform cells.
- Example: Rous sarcoma virus (RSV) carries src gene.
C. Classification of Oncogenic Viruses
1. DNA Oncogenic Viruses
| Virus Family | Virus | Associated Cancer |
| Papillomaviridae | Human papillomavirus (HPV types 16, 18) | Cervical, anal, oral cancers |
| Hepadnaviridae | Hepatitis B virus (HBV) | Liver cancer |
| Herpesviridae | Epstein–Barr virus (EBV) | Burkitt’s lymphoma, Nasopharyngeal carcinoma |
| Kaposi’s sarcoma–associated herpesvirus (KSHV/HHV-8) | Kaposi’s sarcoma | |
| Adenoviridae | Adenoviruses (in animals) | Experimental tumors in rodents |
2. RNA Oncogenic Viruses
| Virus Family | Virus | Associated Cancer |
| Retroviridae | Human T-cell leukemia virus type I (HTLV-1) | Adult T-cell leukemia |
| Rous sarcoma virus (RSV, in chickens) | Sarcoma | |
| Flaviviridae | Hepatitis C virus (HCV) | Hepatocellular carcinoma |
D. Viral Genes Involved in Oncogenesis
| Gene | Function | Example |
| v-onc | Viral oncogene that induces cell growth | RSV (src gene) |
| E6, E7 | Inactivate tumor suppressors p53 and Rb | HPV |
| Tax | Activates cellular proliferation genes | HTLV-1 |
| LMP1 | Activates B-cell proliferation | EBV |
E. Examples of Virus-Induced Cancers
| Virus | Cancer Type | Mechanism |
| HPV (Human papillomavirus) | Cervical, anal, head & neck cancers | Inactivation of p53, Rb |
| HBV & HCV | Hepatocellular carcinoma | Chronic inflammation, integration |
| EBV | Burkitt’s lymphoma, Hodgkin’s lymphoma | B-cell activation |
| KSHV (HHV-8) | Kaposi’s sarcoma | Expression of viral oncogenes |
| HTLV-1 | Adult T-cell leukemia | Expression of Tax protein |
5. Outcomes of Virus–Cell Interaction
| Outcome | Description | Example |
| Cytolytic infection | Cell destruction after replication | Poliovirus |
| Persistent infection | Continuous virus production without killing cell | Hepatitis B |
| Latent infection | Dormant virus, reactivates periodically | Herpesvirus |
| Transformation | Normal cell becomes malignant | HPV, EBV |
| Abortive infection | Virus enters but fails to multiply | Some adenoviruses |
6. Detection of Viral Transformation
Laboratory indicators of viral transformation include:
- Loss of contact inhibition (cells pile up)
- Altered cell morphology (rounded, refractile)
- Chromosomal abnormalities
- Tumor formation in experimental animals
- Expression of viral antigens on cell surface
7. Prevention and Control
- Vaccination – HPV and HBV vaccines reduce cancer risk.
- Screening programs – For early detection (Pap smears, liver screening).
- Antiviral therapies – Suppress chronic viral replication (e.g., interferon, antivirals).
- Public health measures – Safe blood transfusions, needle safety, sexual hygiene.
