Human Rhinovirus C (HRV-C) Virus Profile – Assignment Brief and Writing Guide

Core Summary

This assignment requires a virus profile on human rhinovirus C (HRV-C) for an introductory microbiology class. The paper must be 700–1100 words, based on at least three primary scientific research articles, and follow specific formatting guidelines. It should describe the virus’s structure, genome, host range, replication cycle, and clinical significance, with particular emphasis on HRV-C’s role in severe pediatric respiratory disease and asthma exacerbations. Students must include at least one recent peer-reviewed publication from within the last five years and demonstrate proper scientific citation in APA or Harvard format.

Assignment Overview

Course: Introductory Microbiology
Subject: Biology
Assignment Type: Research Paper – Virus Profile
Topic: Human Rhinovirus C (HRV-C)
Length: 700–1100 words (excluding reference page)
Formatting: Double-spaced, Times New Roman, size 12 font, 1-inch margins
Deadline: 07.03.2018 22:00

Assignment Description

This paper is a virus profile on human rhinovirus C (HRV-C) for your introductory microbiology class. It should be completely based on primary scientific research articles (at least three sources required, though you may use more). The paper is intended to describe the virus and provide details about why the microbe is interesting or has an impact on humans, the environment, or industry. Structural information, host range, and aspects of the life cycle and replication should be included. You must discuss at least one aspect that might be interesting to others in terms of health, industry, or the environment. Relevant information must be drawn from at least one recent peer-reviewed scientific publication published within approximately the last five years.

Key Requirements

Content Requirements

• Describe the virus’s morphology and structural features (icosahedral capsid, non-enveloped nature, genome type)
• Indicate genome type: positive-sense single-stranded RNA (+ssRNA)
• Include host information and cell tropism (ciliated airway epithelial cells via CDHR3 receptor)
• Explain the replication cycle and life cycle stages
• Discuss at least one health, environmental, or industrial impact
• Reference at least one peer-reviewed publication from within the last five years

Formatting Requirements

• 700–1100 words (excluding reference page)
• Double-spaced throughout
• Times New Roman, size 12 font
• 1-inch margins on all sides
• Student name and number provided on title page
• Paragraphs clearly indicated (indent first line or include blank line above)
• Page numbers at top or bottom of pages
• Consistent use of font
• Appropriate title included

Grading Rubric

Structure and Format (2 marks)

2 marks: Word count provided and within limits; double-spaced; margins at least 1 inch; student name and number provided; paragraphs clearly indicated; appropriate title; page numbers present; consistent font use.

1 mark: As above, but with 1–2 formatting errors or word count slightly outside limits (within 10 words).

0.5 marks: 3–4 formatting errors or word count exceeded by more than 10 words.

0 marks: Multiple errors beyond those listed above.

Content (4 marks)

4 marks: Complete, correct, and interesting information provided. Description includes major characteristics (morphology, structural features, lifestyle/replication). Genome type correctly indicated. Appropriate use of scientific resources. At least one health, environmental, or industrial aspect fully explained and accurately represented.

3 marks: Less comprehensive; items above less consistently represented (e.g., health aspect mentioned but not fully explained).

2 marks: Missing some key information or lacking health/environmental/industrial aspect; irrelevant information may be included.

1 mark: Minimal information; scientific errors; irrelevant or misleading information.

0 marks: Understanding of topic not demonstrated.

Writing (3 marks)

3 marks: Written well. References relevant and cited appropriately. Written at appropriate level for scientific audience. Logical organization and flow. All scientific names formatted correctly. No grammar or spelling errors.

2 marks: As above but less consistent (e.g., 1–3 grammar/spelling errors).

1 mark: Lacks clear logical organization; more than 3 grammar/style/format errors.

0 marks: Many errors; difficult to understand; poor presentation.

Referencing and Citations (2 marks)

2 marks: References section includes all references in requested format, listed alphabetically by last name of first author; all authors listed in same order as original source; scientific and gene names formatted correctly; single-spaced entries with entries separated by a line.

1 mark: References listed but with 1–3 errors.

0 marks: References listed with many errors.

Research, Writing, Citation and Referencing Guide

Research Approach

Begin by locating primary research articles on HRV-C through PubMed, Google Scholar, or your university library database. Focus on articles that describe the virus’s molecular characteristics, replication mechanisms, and clinical significance. At minimum, you should reference:

• One article on HRV-C structure or genome organization
• One article on HRV-C replication or receptor binding
• One article on HRV-C clinical impact or disease associations

Writing Tips

Organize your paper with a clear introduction that presents HRV-C and its significance, followed by sections on viral structure and genome, host range and cell tropism, replication cycle, and finally a discussion of health impact. Use precise scientific terminology and maintain an objective, evidence-based tone. Avoid conversational language and ensure all claims are supported by citations.

Citation Style

Use APA 7th Edition or Harvard referencing format consistently throughout. In-text citations should include author last name and year of publication. The reference list should be alphabetized by the first author’s last name and include DOIs where available.

Common Pitfalls to Avoid

• Relying solely on review articles or textbook sources instead of primary research
• Failing to include at least one recent publication (within five years)
• Neglecting to specify the genome type (+ssRNA) for the virus
• Overlooking the health impact section or providing superficial discussion
• Incorrect formatting of scientific names and gene names

Sample Answer Excerpt: HRV-C Structure and Receptor Tropism

Human rhinovirus C (HRV-C) is a non-enveloped, positive-sense single-stranded RNA virus belonging to the family Picornaviridae. The viral capsid adopts an icosahedral structure composed of 12 pentamers, with a diameter of approximately 30 nanometers. The genome is approximately 7.4 kilobases in length and contains a single open reading frame encoding a polyprotein that is cleaved into structural and non-structural proteins. A distinctive feature of HRV-C is its use of cadherin-related family member 3 (CDHR3) as the cellular receptor, which distinguishes it from HRV-A and HRV-B species that utilize intercellular adhesion molecule-1 (ICAM-1) and low-density lipoprotein receptors, respectively. CDHR3 is expressed on the apical surface of ciliated airway epithelial cells, giving HRV-C a more restricted cell tropism compared to other rhinovirus species. A coding single-nucleotide polymorphism in CDHR3 (rs6967330, C529Y) has been linked to increased cell-surface receptor expression and approximately tenfold higher viral binding and progeny yields, which may explain why certain individuals are more susceptible to severe HRV-C infections. This receptor specificity not only shapes the virus’s pathogenesis but also presents a unique target for therapeutic intervention.

Clinical Significance and Asthma Connection

HRV-C is now recognized as the most common cause of acute wheezing exacerbations in young children presenting to hospitals. Among hospitalized children with virus-induced asthma exacerbations, HRV-C accounts for over half of all rhinovirus detections, making it the predominant viral trigger for severe pediatric respiratory disease. The association between HRV-C and asthma extends beyond acute exacerbations. A multicenter prospective study of U.S. infants hospitalized for bronchiolitis found that only infants with HRV-C infection had a significantly higher risk of physician-diagnosed asthma at four years of age. The CDHR3 C529Y variant has been consistently linked to more severe clinical outcomes, including earlier age of asthma onset and more frequent hospitalizations. Recent research using primary human airway epithelial cultures has demonstrated that RV-C15 infection induces significant disruptions in ciliary function, reduces ciliary beat frequency, and promotes mucus hypersecretion through upregulation of FOXA3 and MUC5AC expression. These findings suggest that HRV-C’s pathogenic potential lies not only in its ability to evade immune detection but also in its capacity to remodel the airway epithelium and compromise mucociliary clearance.

Advancing HRV-C Research Through Novel Model Systems

The study of HRV-C has historically been hampered by the virus’s poor or absent replication in standard cell lines. This technical limitation has driven the development of innovative model systems. A 2024 study published in Nature Communications demonstrated that human respiratory organoids can sustain reproducible propagation of HRV-C, with nasal organoids achieving this without immunosuppression. This organoid-based system has enabled comprehensive characterization of virus-host interactions, including the observation that airway organoids mount a stronger innate immune response to HRV-C infection compared to nasal organoids. Treatment with anti-CDHR3 antibodies and antiviral compounds significantly reduced viral growth in both airway and nasal organoids, validating the model for drug discovery applications. The development of these physiologically active models opens new avenues for propagating other uncultivable human and animal viruses, representing a significant advance for virology research. This technological progress may ultimately facilitate the development of targeted antivirals against HRV-C, addressing a major unmet need in pediatric respiratory medicine.

Why HRV-C Research Matters in Clinical Practice

The clinical significance of HRV-C extends beyond the pediatric population. While children bear the greatest burden of severe disease, emerging evidence indicates that HRV-C also contributes to significant morbidity in adults, particularly those with underlying asthma or immunocompromising conditions. The identification of CDHR3 as the viral receptor has provided a molecular explanation for host susceptibility and offers a rational target for preventive strategies. Genotyping of CDHR3 single-nucleotide polymorphisms may help physicians formulate prediction models for the severity of rhinovirus-associated respiratory tract infections. Furthermore, the development of antiviral compounds targeting the highly conserved 3C protease, such as rupintrivir, shows promise for therapeutic intervention. However, the genetic diversity within HRV-C species, with over 57 genotypes identified, presents ongoing challenges for vaccine development and antiviral efficacy. Understanding the molecular basis of HRV-C pathogenesis remains essential for reducing the global burden of virus-induced asthma and severe respiratory illness.

Frequently Asked Question

What distinguishes human rhinovirus C from other rhinovirus species, and why does this matter for disease severity?

Human rhinovirus C is distinguished from HRV-A and HRV-B by its unique cellular receptor, CDHR3, which is expressed on ciliated airway epithelial cells. Unlike HRV-A and HRV-B, which use ICAM-1 and LDL receptors respectively, HRV-C’s use of CDHR3 restricts its tropism to ciliated cells of the respiratory tract. This receptor specificity has significant clinical implications. A coding variant in CDHR3 (rs6967330, C529Y) increases cell-surface receptor expression and is associated with a tenfold increase in viral binding and replication. Children carrying this variant are more susceptible to severe HRV-C infections, asthma exacerbations, and recurrent hospitalizations. The clinical importance of this distinction is underscored by findings that HRV-C is the most common cause of acute wheezing in hospitalized young children and is uniquely associated with subsequent asthma development. Understanding these species-specific differences is crucial for developing targeted therapeutic strategies and identifying children at highest risk for severe disease.

Recommended References

Bochkov YA, Watters K, Ashraf S, et al. (2015). Cadherin-related family member 3, a childhood asthma susceptibility gene product, mediates rhinovirus C binding and replication. Proceedings of the National Academy of Sciences, 112(17), 5485-5490. https://doi.org/10.1073/pnas.1421178112

Li C, Yu Y, Wan Z, et al. (2024). Human respiratory organoids sustained reproducible propagation of human rhinovirus C and elucidation of virus-host interaction. Nature Communications, 15(1), 10772. https://doi.org/10.1038/s41467-024-55076-2

Li Y, Singh S, et al. (2025). Rhinovirus C15 infection induces airway epithelial cell remodeling and robust inflammatory responses: Potential implications for airway obstruction in children. Mucosal Immunology, 18(6), 1341-1352. https://doi.org/10.1016/j.mucimm.2025.09.003

Alsayed AR, Abed A, Al Shawabkeh MJ, et al. (2024). Human Rhinovirus: Molecular and Clinical Overview. Pharmacy Practice, 22(1), 1-11. https://www.pharmacypractice.org/index.php/pp/article/view/2925

Yuan S, Fan K, Chen Z, et al. (2020). Structure of the HRV-C 3C-Rupintrivir Complex Provides New Insights for Inhibitor Design. Virologica Sinica, 35, 445-454. https://doi.org/10.1007/s12250-020-00196-4

Pediatric and adult primary human airway epithelia exhibit similar rhinovirus C replication, innate responses, and expression of protein receptor. (2026). Microbiology Spectrum. https://journals.asm.org/doi/10.1128/spectrum.01611-26

Next Week’s Assignment (Week 4)

Topic: Virus Profile – Influenza A Virus
Description: Write a virus profile on Influenza A virus covering its segmented genome, antigenic shift and drift mechanisms, host range, and seasonal impact. Include discussion of vaccination strategies and antiviral resistance. Length: 700–1100 words. Reference at least three primary research articles with at least one from the last five years.
Formatting: Double-spaced, Times New Roman, size 12, 1-inch margins. APA 7th Edition referencing.
Deadline: