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Effect of viruses and interferon on chick embryo otocyst cultures
1Department of Otolaryngology-Head and Neck Surgery, Johns Hopkins Medical Institutions, Baltimore, Maryland.
Abstract:
Chick embryo otocyst organ cultures were subjected to live vesicular stomatitis virus and rubella virus preparations, to interferon (IFN), and to a combination of both virus and IFN, and compared to control untreated otocysts. We observed morphologic and microscopic changes suggestive of individual cell death and delayed organ differentiation in the virus-treated groups, along with an appreciable decrease in size of the otocyst. Low-dose IFN treatment prior to virus inoculation appeared to partially prevent these effects. The addition of IFN alone did not seem to affect the differentiation process. Time-lapse videophotography further confirmed the above findings. This study suggests that the peripheral component of congenital deafness associated with viral infections is likely to be an effect of the virus itself, and not of the IFN. Interferon provides a partial protective effect against the insult from the virus in vitro and does not seem to be toxic to the developing otocyst.
Insights
Viral infections in developing chick otocysts cause cell death and delayed differentiation. Interferon (IFN) partially protects against these effects without harming the otocyst, suggesting viruses, not IFN, cause congenital deafness.
Area of Science:
- Developmental Biology
- Virology
- Oto-toxicology
Background:
- Congenital deafness can be associated with viral infections during development.
- The role of viral infections and the body's immune response, specifically interferon (IFN), in inner ear development is not fully understood.
Purpose of the Study:
- To investigate the effects of vesicular stomatitis virus and rubella virus on chick embryo otocyst development in vitro.
- To determine the protective role of interferon (IFN) against viral-induced damage in the developing otocyst.
- To elucidate whether the virus or IFN is responsible for potential peripheral defects leading to congenital deafness.
Main Methods:
- Chick embryo otocyst organ cultures were exposed to live viruses (vesicular stomatitis virus, rubella virus), interferon (IFN), or a combination.
- Morphological and microscopic changes were assessed.
- Time-lapse videophotography was employed to observe cellular dynamics.
- Control untreated otocysts were used for comparison.
Main Results:
- Virus exposure led to cell death, delayed differentiation, and reduced otocyst size.
- Low-dose IFN pretreatment partially mitigated virus-induced damage.
- IFN alone did not impede otocyst differentiation.
- IFN demonstrated a partial protective effect against viral insult in vitro without apparent toxicity.
Conclusions:
- The peripheral component of congenital deafness linked to viral infections is likely caused by the virus itself, not by the host's interferon response.
- Interferon offers partial protection against viral damage to the developing otocyst in vitro.
- Interferon does not appear to be toxic to the developing otocyst, suggesting a potential therapeutic window.
