Need to characterise strains from Carrier Pigs and find out their clinical impact in naive pigs.
I think this has to do with the pathogenicity of the virus as well as other intrinsic factors of the host and its response to the virus. Naturally, we observe some degree of resistance in our local pigs relative to the thorough breeds which has to do with their genetic make up. But also there could be factors that could play in the host being either resistant or highly susceptibe at the time of exposure to the virus. Individual immunity among groups could be a factors, other predisposing factors could play a role as well.
Dear William, thanks for your observation and question. We are dealing (apparently) with the same ASF genotype IX in Uganda. We are currently carrying out full genome sequence of the ASF genotype IX to see if there are unique differences that could point towards variations in pathogenicity/severity of infection. From the host's perspective, we need to investigate the pathology/pathogenesis (how does disease progress, what systems are affected and to what extent); and also we are carrying out genomic comparisons among domestic/local pigs and wild pigs. We need a concerted and uninterrupted research drive.
Charles and Lazarus have provided perspectives to which I want to comment upon. Perhaps there are intrinsic factors associated with the pig genes. Remember that the improved breeds originated from the European wild pig which is linked to European wild boars and both are quite susceptible. However other pig types hardly come down significantly with infection.
I agree with the above answers. Unfortunately we are very far from knowing the answer to the question, although research is ongoing in various institutions. However, that pig factors are involved is certain, because a virus that is extremely virulent and able to cause severe ASF with high mortality in some pigs while apparently not affecting others, e.g. in endemic areas, cannot be accused of loss of virulence. It would be interesting to examine the level of exposure that occurs in areas like Angonia in Mozambique and Homabay in Kenya, where pig populations have shown unexpectedly survival rates with no signs of chronic disease, when the pigs are very young or the sows are pregnant. We know that the antibodies to ASFV last for a long time so it may be possible that pigs exposed, maybe to sublethal doses of virus, when they have passive immunity could be protected against future attacks. It would be a difficult task to investigate this, however, as it has to be done under natural conditions.
Dear Colleagues,
Thanks for the Observations. Certainly there are intrinsic and extrinsic factors. For example, there was an outbreak of ASF in Wakiso, Uganda, in the village where I live. Of my 7 piglets kept in a cubicle, five died including the sow and 2 survived !!. Dr Afayoa tested the 2 for Abs and titres were high. Unfortunately we never isolated the virus. Secondly, in a Sandwich ASF Antigen- ELISA test developed by Dr Afayoa and I, we observed a very significant background in OD values of negative controls from Japanese Pigs (negligible background) and Ugandan pigs raised under ASF-free condithions (high background). This could be attributed to the degree of exposure to the virus and carrier state. Thirdly, We also need to investigate why such paractute syndromes should occur in the midst of endemicity as often observed in Uganda. A combination of molecular, serological and Pathological studies could yield some answer. For example in Uganda wit IX genotype could the virus be mutating at sub IX level? My thinking is that there could be sub-geno types and sub-serotypes. Molecular Biology studies could address this in combination with virus neutralising studies using a panel of Monoclonal antibodies against the identified strains to identify patterns of cross-reactivity.
William Olaho-Mukani
An interesting answer. Bear in mind that DNA viruses, unlike RNA viruses, are stable viruses. Certainly small mutations occur at molecular level to allow us to type ASF viruses at subgeneric level, but so far we have little evidence that these small changes have any influence on the biology of the virus.
At present ASF viruses are treated as belonging to a single serotype, because most attempts to classify them into serotypes have not been successful. Research on this is ongoing, look out for publications by Dr Alexander Malogolovkin on the work he has done in Russia on identification of serotypes for ASF,
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