Rhinovirus

Last updated: November 01, 2022

Rhinovirus

Watch later

Watch later

Action potentials in myocytes
Action potentials in pacemaker cells
Excitability and refractory periods
Cardiac excitation-contraction coupling
Antidiuretic hormone
Calcitonin
Phosphate, calcium and magnesium homeostasis
Vitamin D
Blood components
Innate immune system
Complement system
Cytokines
T-cell development
B-cell development
MHC class I and MHC class II molecules
T-cell activation
B-cell activation, differentiation, and contraction
Cell-mediated immunity of CD4 cells
Cell-mediated immunity of natural killer and CD8 cells
B- and T-cell memory
Type I hypersensitivity
Type II hypersensitivity
Type III hypersensitivity
Type IV hypersensitivity
Bone remodeling and repair
Muscular system anatomy and physiology
Neuromuscular junction and motor unit
Slow twitch and fast twitch muscle fibers
Muscle spindles and golgi tendon organs
Muscle contraction
Sliding filament model of muscle contraction
Nervous system anatomy and physiology
Neuron action potential
Adrenergic receptors
Sympathetic nervous system
Parasympathetic nervous system
Cholinergic receptors
Body fluid compartments
Movement of water between body compartments
Hydration
Renin-angiotensin-aldosterone system
Sodium homeostasis
Potassium homeostasis
Osmoregulation
Necrosis and apoptosis
Hypoxia
Ischemia
Inflammation
Wound healing
Oncogenes and tumor suppressor genes
Hyperplasia and hypertrophy
Atrophy, aplasia, and hypoplasia
Metaplasia and dysplasia
Pharmacodynamics: Drug-receptor interactions
Enzyme function
Pharmacodynamics: Agonist, partial agonist and antagonist
Pharmacodynamics: Desensitization and tolerance
Pharmacokinetics: Drug absorption and distribution
Pharmacokinetics: Drug elimination and clearance
Pharmacokinetics: Drug metabolism
Cholinomimetics: Direct agonists
Muscarinic antagonists
Cholinomimetics: Indirect agonists (anticholinesterases)
Sympathomimetics: Direct agonists
Sympatholytics: Alpha-2 agonists
Adrenergic antagonists: Presynaptic
Adrenergic antagonists: Alpha blockers
Adrenergic antagonists: Beta blockers
Anticoagulants: Heparin
Anticoagulants: Warfarin
Monoclonal antibodies
Glucocorticoids
Cell wall synthesis inhibitors: Penicillins
Cell wall synthesis inhibitors: Cephalosporins
DNA synthesis inhibitors: Fluoroquinolones
Antimetabolites: Sulfonamides and trimethoprim
DNA synthesis inhibitors: Metronidazole
Mechanisms of antibiotic resistance
Protein synthesis inhibitors: Aminoglycosides
Miscellaneous cell wall synthesis inhibitors
Integrase and entry inhibitors
Protease inhibitors
Nucleoside reverse transcriptase inhibitors (NRTIs)
Azoles
Miscellaneous antifungal medications
Echinocandins
Acetaminophen (Paracetamol)
Non-steroidal anti-inflammatory drugs
Parathyroid conditions and calcium imbalance: Clinical
Parathyroid disorders and calcium imbalance: Pathology review
DNA replication
Transcription of DNA
DNA mutations
Translation of mRNA
Proteins
Resting membrane potential
Demyelinating disorders: Pathology review
Blood groups and transfusions
Microcirculation and Starling forces
Bacterial structure and functions
Staphylococcus epidermidis
Staphylococcus aureus
Staphylococcus saprophyticus
Streptococcus pneumoniae
Clostridium perfringens
Clostridium botulinum (Botulism)
Clostridium tetani (Tetanus)
Clostridium difficile (Pseudomembranous colitis)
Escherichia coli
Salmonella (non-typhoidal)
Enterobacter
Shigella
Vibrio cholerae (Cholera)
Campylobacter jejuni
Mycoplasma pneumoniae
Viral structure and functions
Varicella zoster virus
Human herpesvirus 8 (Kaposi sarcoma)
Epstein-Barr virus (Infectious mononucleosis)
Herpes simplex virus
Human herpesvirus 6 (Roseola)
Adenovirus
Human papillomavirus
Rhinovirus
Influenza virus
Norovirus
Rotavirus
Vaccinations
Immunodeficiencies: Combined T-cell and B-cell disorders: Pathology review
Immunodeficiencies: T-cell and B-cell disorders: Pathology review
Immunodeficiencies: Phagocyte and complement dysfunction: Pathology review
Introduction to the lymphatic system
Mendelian genetics and punnett squares
Inheritance patterns
Muscular dystrophies and mitochondrial myopathies: Pathology review
Autosomal trisomies: Pathology review
Miscellaneous genetic disorders: Pathology review
Independent assortment of genes and linkage
DNA structure
Nuclear structure
Amino acids and protein folding
Gene regulation
Lac operon
Karyotyping
Gel electrophoresis and genetic testing
Polymerase chain reaction (PCR) and reverse-transcriptase PCR (RT-PCR)
DNA cloning
Down syndrome (Trisomy 21)
Huntington disease
Williams syndrome
Cystic fibrosis
Glycogen storage disease type I
Glycogen storage disease type II (NORD)
Glucose-6-phosphate dehydrogenase (G6PD) deficiency
Deep vein thrombosis
Deep vein thrombosis and pulmonary embolism: Pathology review
Immunodeficiencies: Clinical
Selective immunoglobulin A deficiency
Isolated primary immunoglobulin M deficiency
Dermatomyositis
Crohn disease
Complement deficiency
Lupus nephritis
Thymus histology
Lymph node histology
Spleen histology
Respiratory alkalosis

Transcript

Watch video only

Content Reviewers

Human Rhinovirus (HRV) is a communicable, infectious virus that causes inflammation of the nasal mucosa, or rhinitis.

It mainly causes upper respiratory tract infections, and gets its rhino- name, meaning nose, because it commonly causes a runny nose, nasal congestion, and sneezing, as well as a sore throat and cough.

There are over 100 serologic known types and all of them can cause a "common cold” in humans!

Now, rhinovirus belongs to the picornaviridae family of viruses.

They are naked viruses, about 30 nanometers in diameter, and they’re surrounded by an icosahedral capsid, which is a spherical protein shell made up of 20 equilateral triangular faces.

And they’re “naked” because the capsid isn’t covered by a lipid membrane.

They’re also single-stranded, positive-sense ribonucleic acid, or RNA, viruses.

This means that their RNA is actually mRNA, which the host cell ribosomes use to make viral proteins.

Unlike other picornaviruses, rhinoviruses are acid labile.

That means they can be destroyed by stomach acid, so they don’t typically infect the GI tract and don’t spread through a fecal-to-oral route.

On the other hand, rhinoviruses commonly infect the epithelium of the respiratory mucosa, which lines the nasal cavity.

So rhinovirus transmission occurs through contact with infected respiratory secretions, like snot and aerosols, particularly from nose blowing or sneezing.

Touching an infected surface, like a door handle or shaking hands, and then touching an uninfected respiratory mucosa is a main way to transfer an infection - that’s because rhinoviruses can survive up to 2 hours on the skin, and 4 days on surfaces.

Once rhinovirus has been introduced to the respiratory mucosa, it targets cell surface receptors expressed at the surface of nasal epithelial cells.

Rhinoviruses can target a few specific receptors for entry, but one in particular is intercellular adhesion molecule-1, or ICAM-1.

This attachment allows for rhinovirus to be eaten, or endocytosed, into the host cell.

During the endocytosis process, the icosahedral capsid breaks open, allowing the single stranded RNA of Rhinovirus to gain access to the host cell cytoplasm.

In the cytoplasm, the host cell ribosomes take over viral protein production, helping the virus replicate.

Key Takeaways

Rhinovirus is a type of virus that causes the common cold. It infects the epithelium of the respiratory mucosa, typically through a nasal route of transmission. The result is an inflammatory response from immune cells, which leads to a runny nose, nasal congestion, sneezing, and sore throat. Diagnosis is usually made clinically, and the treatment focuses on symptom relief and preventing the spread of infection to others. To prevent the spread of rhinovirus, it is important to practice good hygiene, such as washing your hands frequently and avoiding close contact with people who are sick.