As you know vacoulation in CNS would be a typical lesion in VNN disease that was appeared more in adult affected fish.
Dear friends,
Let me ask my question again through other aspect.
According to your opinion with concerning the virus property and pathoghenisity of the occurrence of mentioned lesions, which tissue would be affected at the first? Brain or Retina? which one would be more sensitive? Why?
The Neurotropism of VNN is irrefutable and the nervous tissues like CNS, Spinal cord ,...) because of receptor or coreceptor of cell memmber, are the primary sites for VNN entry and replication.Virus through nasal epithelium penetrate and invade the olfactory nerve cell and replicate there, so pathological changes first developed in the olfactory lobe and spread through the blood brain system and it can reach retina.
Of course must say pathological injuries in viral infections are more due to the host's immune response and their products, and the viral itself has played a lesser role. However, that the type of immune response and its extent depends on a variety of factors, such as changing the host environment, the stress and the frequency of exposure to the host with virus, so sometimes, with the presence of a viral agent and host immune system, the clinical signs are not visible, but the change of the target tissue of the virus is observed.
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Hi
according to articles and my idea, first brain gets infected and it also is the more sensitive.on the other hand Cellular immunity with T lymphocyte and their production lead to the destruction of virus-infected cells and, consequently, their vacuation.
best regards
Dear Dr. Ziarati,
Thank you for your valued answers. You are right completely.
Let me present you other experiment that was done by my dear friend, Prof. Chi Shau Chi from National University in Taiwan. She described entrance of the VNN virus as follow:
During naturally acute infection, small amount of NNV was first detectable in the spinal cord at the position above swim bladder in 3 out of 39 larvae examined as 0 day old, then all the nervous tissues and the epithelial layer of the gill operculum, the oral cavity and the skin of 1 day old larvae. The intensity of IFA staining increased in nerve tissues of 2 day old larvae while it remained moderate in the skin. By TEM observation, virions were found either in the nerve tissues or in the hyperplastic epithelial cells of skin of 1-2 day old larvae.
It is suggested that the initial multiplication site of NNV is spinal cord, particular the area above swimbladder. From this area, virus spread backward to the end of spinal cord and forward to the brain, and ended in the retina.
It is possible that virus enters the host via the skin or grastrointestinal epithelium, and virus in the epithelium is a transient infection instead of productive infection. The presence of NNV in epithelium could be a result of systemic infection or alternatively epithelial cells of the skin may be susceptible to NNV only in the very early development stage. NNV exhibits neuron tropism suggested that the virus entered the spinal cord via sensory and/or motor nerve cells linked to the epithelium.
However, IFA positive staining was not found in the skin of 3-6 day old larvae during naturally subacute infection, nor in 12-72 hr old larvae after NNV bath challenge.
However, the role of skin as a portal of entry of SJNNV remains unclear.
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