Viral interference

Short description: Inhibition of virus growth caused by previous exposure of cells to another virus

Viral interference, also known as superinfection resistance,[1] is the inhibition of viral reproduction caused by previous exposure of cells to another virus.[2] The exact mechanism for viral interference is unknown.[3] Factors that have been implicated are the generation of interferons by infected cells,[4] and the occupation or down-modulation of cellular receptors.[1]

## Contents

* 1 Overview
* 2 Examples
* 2.1 Bacteriophage T4
* 2.2 Respiratory viruses
* 2.3 Live-attenuated vaccines
* 3 History
* 3.1 2009 influenza pandemic
* 3.2 COVID-19 pandemic
* 4 References

## Overview

Viral interference is considered the most common outcome of coinfection, or the simultaneous infection of a host by two or more distinct viruses.[5] The primary form of viral interference is known as superinfection exclusion, in which the initial infection stimulates a resistance to subsequent infection by related viruses.[5][6] Interference can occur as well in the form of superinfection suppression, in which persistently infected cells hold off infection by unrelated viruses. Viral interference has also been observed to occur in the use of vaccines containing live-attenuated viruses, in both directions — in some cases vaccines disrupting viruses unrelated to those they were targeting, and in others wild viruses rendering vaccines of this kind less effective.[5]

## Examples

### Bacteriophage T4

A primary infection by bacteriophage (phage) T4 of its E. coli host ordinarily leads to genetic exclusion of a secondarily infecting phage, preventing the secondary phage from contributing its genetic information to progeny. This viral interference depends on the expression by the primary phage of the genes immunity (imm) and spackle (sp).[7][8] The imm gp appears to enable the host exonuclease V to degrade the superinfecting phage DNA, and the sp gp appears to interfere with the DNA injection process of secondary phage.[8] If the primary infecting phage is subjected to DNA damaging treatment prior to infection, this treatment tends to permit entry of the secondary phage's DNA, thus shifting reproduction from an asexual to a sexual mode and allowing rescue of the primary phage's genes.[9]

### Respiratory viruses

Interference has been observed to occur among endemic respiratory viruses. For example, human rhinovirus (HRV) infection has been shown to reduce the likelihood of codetection of other respiratory viruses, suggesting that it may confer a protective effect against other viruses such as influenza.[10] The mechanism at play here has been suggested to be the expression of interferon-stimulated genes in the "target tissue" of HRV infection — the epithelium of the airway, where there has been observed to be an "unexpected high prevalence" of the virus, even among asymptomatic individuals.[11][12] This process thus stimulates an antiviral state, shielding nearby cells from further infection.[10] This potential interplay between viruses such as HRV and influenza may be one factor contributing to the timing and severity of their separate though overlapping "seasons".[13][11]

Interference has been reported between respiratory viruses in non-human animals as well, such as between avian influenza viruses and Newcastle disease virus in chicken, turkeys, and ducks.[14][15]

### Live-attenuated vaccines

The first smallpox vaccine, developed by Edward Jenner, used cowpox to prevent smallpox infection.[6] Indeed, the term "vaccine" comes from the Latin phrase variolae vaccinae, Jenner's name for cowpox.[16]

Live enterovirus vaccines have been found to disrupt the spread of various unrelated respiratory viruses, such as influenza, HRV, and respiratory syncytial virus (RSV), in addition to poliovirus (itself an enterovirus), a phenomenon attributed to viral interference.[17] Similarly, during mass immunization campaigns against polio, vaccination seemed to confer some protection against unrelated enteroviruses as well. At the same time, enteroviruses were also found to interfere with the vaccines themselves, leading to instances of vaccine failure.[5]

## History

Viral interference was observed as early as the 16th century. However, it was not until the 20th century that it was described in detail, following experiments involving plants in 1929, animals in 1935, and bacteriophages in 1942.[6]

### 2009 influenza pandemic

The emergence of a novel influenza A virus (pandemic H1N1/09) in early 2009 afforded the opportunity to study how pandemic influenza and seasonal respiratory viruses might interact, placing the concept of viral interference "on more solid footing."[17][18] The virus quickly spread across both the Northern and Southern Hemispheres through the middle of the year. While this is an unusual time for influenza activity in the north, the first wave of the pandemic in the south occurred during the typical influenza period. The pandemic virus quickly became the dominant strain of influenza, largely displacing the seasonal ones in many countries; however, complete replacement was not observed.[19] Ultimately, activity generally peaked at the expected time for influenza in the Southern Hemisphere.[20]

Despite the rapid spread around the world through the middle of the year, the pandemic remained in a lull during the summer in the north following an explosive outbreak in the spring.[21] As predicted, the virus returned in epidemic proportions in the fall, earlier than the typical flu season but at a time when respiratory illnesses are known to become more prevalent. However, in countries such as Sweden, Norway, and France, the epidemic was "delayed" relative to its timing in other countries, such as the United States and Italy. This difference was attributed by some observers to a rhinovirus epidemic that broke out upon the reopening of schools, effectively "delaying" the rise in H1N1 cases until October.[22][23][24] Studies on this potential interaction between HRV and the pandemic influenza at times came to divergent conclusions, however.[25] While this "delay" in countries like Sweden was real (i.e., temporally speaking, the epidemic was later than in other places), studies also showed that coinfections were relatively common and that there was active cocirculation of the two viruses.[25][26][27]

A systematic analysis of studies from 26 countries found that the influenza epidemic delayed the onset of RSV activity by an average of 0.58 months to 2.5 months. The effect was more pronounced in the Northern Hemisphere as compared to the Southern Hemisphere, perhaps due to the timing of the influenza outbreak relative to the period of typical RSV activity in each region; the tropics, meanwhile, experienced minimal delay. This impact persisted into the second RSV season after the start of the pandemic, albeit to a lesser degree, and was no longer observed by the third season.[28]

### COVID-19 pandemic

During the COVID-19 pandemic, the circulation of many respiratory viruses changed dramatically. Amid the rapid global spread of the pandemic SARS-CoV-2 throughout 2020, these viruses, including influenza, fell to historically low levels. Influenza activity remained virtually nonexistent into 2021,[29] when it began to be detected more frequently, but was still low during the 2021–2022 flu season.[30] RSV activity was similarly depressed during the first year of the pandemic, before resurging in 2021.[31] By contrast, cases of HRV and respiratory enteroviruses declined at the onset of the pandemic but soon returned to prepandemic levels, circulating relatively normally.[30]

The above reductions have generally been attributed to the imposition of non-pharmaceutical interventions, such as social distancing, mask use, and school closures.[32][17][33] However, viral interference has also been suggested as the driving force, or at least another driving force, behind this major decline in viral activity, based in part on the experience of the 2009 pandemic.[34][32][35][33] For example, in the winter of 2021–2022, during the surge of the highly transmissible Omicron variant of SARS-CoV-2 in the United States, influenza activity plummeted as the pandemic wave grew, peaking again in the spring once Omicron had subsided.[33][36] A similar phenomenon was observed in Hong Kong in March 2022, when other respiratory viruses "disappeared" during the surge before returning in April.[18] With respect to HRV and respiratory enteroviruses, whose behavior was evidently less affected during the pandemic, an apparent interplay between these and SARS-CoV-2, possibly mediated by viral interference, was identified in some places, such as California and South Korea. Although these viruses continued to circulate at near prepandemic levels, they were found to peak when SARS-CoV-2 activity was low and to decline as SARS-CoV-2 activity increased.[30]

## References

1. ↑ 1.0 1.1 Remion, Azaria; Delord, Marc; Saragosti, Sentob; Mammano, Fabrizio (2013-09-19). "Co-infection, super-infection and viral interference in HIV". Retrovirology 10 (1): 59–67. doi:10.1186/1742-4690-10-S1-P72. ISSN 1742-4690. PMID 26499042.
2. ↑ Schultz-Cherry, Stacey (2015-12-01). "Viral Interference: The Case of Influenza Viruses" (in en). The Journal of Infectious Diseases 212 (11): 1690–1691. doi:10.1093/infdis/jiv261. ISSN 0022-1899. PMID 25943206.
3. ↑ Laurie, Karen L.; Horman, William; Carolan, Louise A.; Chan, Kok Fei; Layton, Daniel; Bean, Andrew; Vijaykrishna, Dhanasekaran; Reading, Patrick C. et al. (2018-01-30). "Evidence for Viral Interference and Cross-reactive Protective Immunity Between Influenza B VirusLineages" (in en). The Journal of Infectious Diseases 217 (4): 548–559. doi:10.1093/infdis/jix509. ISSN 0022-1899. PMID 29325138.
4. ↑ Dianzani, F. (July 1975). "Viral interference and interferon". La Ricerca in Clinica e in Laboratorio 5 (3): 196–213. doi:10.1007/BF02908284. ISSN 0390-5748. PMID 778995.
5. ↑ 5.0 5.1 5.2 5.3 Kumar, N.; Sharma, S.; Barua, S.; Tripathi, B. N.; Rouse, B. T. (October 2018). "Virological and Immunological Outcomes of Coinfections". Clinical Microbiology Reviews 31 (4). doi:10.1128/CMR.00111-17. PMID 29976554.
6. ↑ 6.0 6.1 6.2 Escobedo-Bonilla, César Marcial (2021). "Mini Review: Virus Interference: History, Types and Occurrence in Crustaceans". Frontiers in Immunology 12. doi:10.3389/fimmu.2021.674216. PMID 34177916.
7. ↑ Cornett, James B. (1974). "Spackle and Immunity Functions of Bacteriophage T4". Journal of Virology 13 (2): 312–321. doi:10.1128/JVI.13.2.312-321.1974. PMID 4589853.
8. ↑ 8.0 8.1 Obringer, John W. (1988). "The functions of the phage T4 immunity and spackle genes in genetic exclusion". Genetics Research 52 (2): 81–90. doi:10.1017/s0016672300027440. PMID 3209067.
9. ↑ Bernstein, Carol (1987). "Damage in DNA of an infecting phage T4 shifts reproduction from asexual to sexual allowing rescue of its genes". Genetics Research 49 (3): 183–189. doi:10.1017/s0016672300027063. PMID 3623097.
10. ↑ 10.0 10.1 Greer, R. M.; McErlean, P.; Arden, K. E.; Faux, C. E.; Nitsche, A.; Lambert, S. B.; Nissen, M. D.; Sloots, T. P. et al. (May 2009). "Do rhinoviruses reduce the probability of viral co-detection during acute respiratory tract infections?". Journal of Clinical Virology 45 (1): 10–15. doi:10.1016/j.jcv.2009.03.008. PMID 19376742.
11. ↑ 11.0 11.1 Wu, A.; Mihaylova, V. T.; Landry, M. L.; Foxman, E. F. (October 2020). "Interference between rhinovirus and influenza A virus: a clinical data analysis and experimental infection study". The Lancet 1 (6): 254–262. doi:10.1016/s2666-5247(20)30114-2. PMID 33103132.
12. ↑ Kiseleva, I.; Ksenafontov, A. (2021). "COVID-19 Shuts Doors to Flu but Keeps Them Open to Rhinoviruses". Biology 10 (8): 733. doi:10.3390/biology10080733. PMID 34439965.
13. ↑ Tanner, H.; Boxall, E.; Osman, H. (2012). "Respiratory viral infections during the 2009–2010 winter season in Central England, UK: incidence and patterns of multiple virus co-infections". European Journal of Clinical Microbiology & Infectious Diseases 31 (11): 3001–3006. doi:10.1007/s10096-012-1653-3. PMID 22678349.
14. ↑ Costa-Hurtado, M.; Afonso, C. L.; Miller, P. J.; Spackman, E.; Kapczynski, D. R.; Swayne, D. E.; Shepherd, E.; Smith, D. et al. (6 January 2014). "Virus interference between H7N2 low pathogenic avian influenza virus and lentogenic Newcastle disease virus in experimental co-infections in chickens and turkeys". Veterinary Research 45 (1): 1. doi:10.1186/1297-9716-45-1. PMID 24393488.
15. ↑ Pantin-Jackwood, M.; Costa-Hurtado, M.; Miller, P. J.; Afonso, C. L.; Spackman, E.; Kapczynski, D.; Shepherd, E.; Smith, D. et al. (15 May 2015). "Experimental co-infections of domestic ducks with a virulent Newcastle disease virus and low or highly pathogenic avian influenza viruses". Veterinary Microbiology 177 (1–2): 7–17. doi:10.1016/j.vetmic.2015.02.008. PMID 25759292.
16. ↑ Baxby, D. (February 1999). "Edward Jenner's Inquiry; a bicentenary analysis". Vaccine 17 (4): 301–307. doi:10.1016/s0264-410x(98)00207-2. PMID 9987167. https://www.sciencedirect.com/science/article/abs/pii/S0264410X98002072.
17. ↑ 17.0 17.1 17.2 Piret, J.; Boivin, G. (February 2022). "Viral Interference between Respiratory Viruses". Emerging Infectious Diseases 28 (2): 273–281. doi:10.3201/eid2802.211727. PMID 35075991.
18. ↑ 18.0 18.1 Cohen, J. (18 November 2022). "Competition between respiratory viruses may hold off a 'tripledemic' this winter". Science. https://www.science.org/content/article/competition-between-respiratory-viruses-may-hold-tripledemic-winter.
19. ↑ Opatowski, L.; Fraser, C.; Griffin, J.; de Silva, E.; Van Kerkhove, M. D.; Lyons, E. J.; Cauchemez, S.; Ferguson, N. M. (September 2011). "Transmission Characteristics of the 2009 H1N1 Influenza Pandemic: Comparison of 8 Southern Hemisphere Countries". PLOS Pathogens 7 (9). doi:10.1371/journal.ppat.1002225. PMID 21909272.
20. ↑ "Differing patterns of influenza activity in the southern hemisphere during and between the 2009 pandemic and the 2010 winter influenza season – the usefulness for Europe". European Centre for Disease Prevention and Control. 4 April 2011. https://www.ecdc.europa.eu/en/news-events/differing-patterns-influenza-activity-southern-hemisphere-during-and-between-2009.
21. ↑ Wilde, J. A. (1 March 2010). "A(H1N1) 'Swine Flu' 2009 / 2010: Where We've Been, What We Now Know, Where We May Be Heading". Pediatric Emergency Medicine Reports. https://www.reliasmedia.com/articles/17564-a-h1n1-swine-flu-2009-2010-where-we-ve-been-what-we-now-know-where-we-may-be-heading. Retrieved 2 May 2024.
22. ↑ Linde, A.; Rotzén-Östlund, M.; Zweygberg-Wirgart, B.; Rubinova, S.; Brytting, M. (8 October 2009). "Does viral interference affect spread of influenza?". Eurosurveillance 14 (40). doi:10.2807/ese.14.40.19354-en. PMID 19822124.
23. ↑ Ånestad, G.; Nordbø, S. A. (December 2011). "Virus interference. Did rhinoviruses activity hamper the progress of the 2009 influenza A (H1N1) pandemic in Norway?". Medical Hypotheses 77 (6): 1132–1134. doi:10.1016/j.mehy.2011.09.021. PMID 21975051. https://www.sciencedirect.com/science/article/abs/pii/S0306987711004749. Retrieved 2024-05-02.
24. ↑ Casalegno, J. S.; Ottmann, M.; Bouscambert Duchamp, M.; Escuret, V.; Billaud, G.; Frobert, E.; Morfin, F.; Lina, B. (1 April 2010). "Rhinoviruses delayed the circulation of the pandemic influenza A (H1N1) 2009 virus in France". Clinical Microbiology and Infection 16 (4): 326–329. doi:10.1111/j.1469-0691.2010.03167.x. PMID 20121829. https://www.clinicalmicrobiologyandinfection.com/article/S1198-743X(14)63294-8/fulltext. Retrieved 2 May 2024.
25. ↑ 25.0 25.1 Rhedin, S.; Hamrin, J.; Naucler, P.; Bunnet, R.; Rotzén-Östlund, M.; Färnert, A.; Eriksson, Margareta (14 December 2012). "Respiratory Viruses in Hospitalized Children with Influenza-Like Illness during the H1n1 2009 Pandemic in Sweden". PLOS ONE 7 (12). doi:10.1371/journal.pone.0051491. PMID 23272110. Bibcode: 2012PLoSO...751491R.
26. ↑ Nisii, C.; Meschi, S.; Selleri, M.; Bordi, L.; Castilletti, C.; Valli, M. B.; Lalle, E. (1 September 2010). "Frequency of Detection of Upper Respiratory Tract Viruses in Patients Tested for Pandemic H1N1/09 Viral Infection". Journal of Clinical Microbiology 48 (9): 3383–3385. doi:10.1128/JCM.01179-10. PMID 20592147.
27. ↑ Esper, F. P.; Spahlinger, T.; Zhou, L. (1 October 2011). "Rate and influence of respiratory virus co-infection on pandemic (H1N1) influenza disease". Journal of Infection 63 (4): 260–266. doi:10.1016/j.jinf.2011.04.004. PMID 21546090. PMC 3153592. https://www.journalofinfection.com/article/S0163-4453(11)00111-3/fulltext. Retrieved 2 May 2024.
28. ↑ Li, Y.; Wang, X.; Msosa, T.; de Wit, F.; Murdock, J.; Nair, H. (4 July 2021). "The impact of the 2009 influenza pandemic on the seasonality of human respiratory syncytial virus: A systematic analysis". Influenza and Other Respiratory Viruses 15 (6): 804–812. doi:10.1111/irv.12884. PMID 34219389.
29. ↑ Peek, K. (29 April 2021). "Flu Has Disappeared for More Than a Year". Scientific American. https://www.scientificamerican.com/article/flu-has-disappeared-worldwide-during-the-covid-pandemic1/.
30. ↑ 30.0 30.1 30.2 Chow, E. J.; Uyeki, T. M.; Chu, H. Y. (17 October 2022). "The effects of the COVID-19 pandemic on community respiratory virus activity". Nature Reviews Microbiology 21 (3): 195–210. doi:10.1038/s41579-022-00807-9. PMID 36253478.
31. ↑ Zheng, Z.; Pitzer, V. E.; Shapiro, E. D. (16 December 2021). "Estimation of the Timing and Intensity of Reemergence of Respiratory Syncytial Virus Following the COVID-19 Pandemic in the US". JAMA Network Open 4 (12): e2141779. doi:10.1001/jamanetworkopen.2021.41779. PMID 34913973.
32. ↑ 32.0 32.1 Avadhanula, V.; Piedra, P. A. (October 2021). "The Prevention of Common Respiratory Virus Epidemics in 2020-21 during the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) Pandemic: An Unexpected Benefit of the Implementation of Public Health Measures". The Lancet Regional Health 2. doi:10.1016/j.lana.2021.100043. PMID 34430955.
33. ↑ 33.0 33.1 33.2 Rubin, R. (21 September 2022). "The Dreaded "Twindemic" of Influenza and COVID-19 Has Not Yet Materialized—Might This Be the Year?". JAMA 328 (15): 1488–1489. doi:10.1001/jama.2022.15062. PMID 36129724.
34. ↑ Greenwood, V. (31 January 2021). "A viral mystery: Can one infection prevent another?". STAT. https://www.statnews.com/2021/01/31/a-viral-mystery-can-one-infection-prevent-another/.
35. ↑ Flam, F. (23 November 2022). "The Real Reasons Your Family Is Sick Right Now". Bloomberg. https://www.bloomberg.com/opinion/articles/2022-11-23/flu-and-rsv-cases-are-up-but-not-covid-infections-what-tripledemic?leadSource=uverify wall.
36. ↑ Krauland, M. G.; Roberts, M. S. (February 2025). "Was Viral Interference Responsible for the Unusual 2021-22 Influenza Season?". Open Forum Infectious Diseases 12 (Supplement_1). doi:10.1093/ofid/ofae631.2493. PMC 11777534. https://academic.oup.com/ofid/article/12/Supplement_1/ofae631.2493/7987813.

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