There was a concordance of 97% between genotype and phenotype. All the heterozygotes had an intermediate phenotype. However, the wide variation range in TPMT activity detected in the wild-type homozygotes indicates that other genetic or epigenetic factors influence the TPMT phenotype.

Nipah virus (NiV) infection is a viral disease caused by a Henipavirus, belonging to the Paramyxoviridae family, responsible for a zoonosis. The course of the disease can be very serious and lead to death. NiV natural hosts are fruit bats (also known as megabats) belonging to the Pteropodidae family, especially those of the Pteropus genus. Natural infection in domestic animals has been described in farming pigs, horses, domestic and feral dogs and cats. Natural NiV transmission is possible intra-species (pig-to-pig, human-to-human) and inter-species (flying bat-to-human, pig-to-human, horse-to-human). The infection can be spread by humans or animals in different ways. It is peculiar how the viral transmission modes among different hosts also change depending on the geographical area for different reasons, including different breeding methods, eating habits and the recently identified genetic traits/molecular features of main virus proteins related to virulence. Outbreaks have been described in Malaysia, Singapore, Bangladesh, India and the Philippines with, in some cases, severe respiratory and neurological disease and high mortality in both humans and pigs. Diagnosis can be made using different methods including serological, molecular, virological and immunohistochemical methods. The cornerstones for control of the disease are biosecurity (via the correct management of reservoir and intermediate/amplifying hosts) and potential vaccines which are still under development. However, the evaluation of the potential influence of climate and anthropogenic changes on the NiV reservoir bats and their habitat as well as on disease spread and inter-specific infections is of great importance. Bats, as natural reservoirs of the virus, are responsible for the viral spread and, therefore, for the outbreaks of the disease in humans and animals. Due to the worldwide distribution of bats, potential new reports and spillovers are not to be dismissed in the future.

The onset of chemotherapy-induced peripheral neurotoxicity (CIPN) is a leading cause of the dose reduction or discontinuation of cancer treatment due to sensory symptoms. Paclitaxel (PTX) can cause painful peripheral neuropathy, with a negative impact on cancer survivors’ quality of life. While recent studies have shown that neuroinflammation is involved in PTX-induced peripheral neurotoxicity (PIPN), the pathophysiology of this disabling side effect remains largely unclear and no effective therapies are available. Therefore, here we investigated the effects of human intravenous immunoglobulin (IVIg) on a PIPN rat model. PTX-treated rats showed mechanical allodynia and neurophysiological alterations consistent with a severe sensory axonal polyneuropathy. In addition, morphological evaluation showed a reduction of intra-epidermal nerve fiber (IENF) density and evidenced axonopathy with macrophage infiltration, which was more prominent in the distal segment of caudal nerves. Three weeks after the last PTX injection, mechanical allodynia was still present in PTX-treated rats, while the full recovery in the group of animals co-treated with IVIg was observed. At the pathological level, this behavioral result was paralleled by prevention of the reduction in IENF density induced by PTX in IVIg co-treated rats. These results suggest that the immunomodulating effect of IVIg co-treatment can alleviate PIPN neurotoxic manifestations, probably through a partial reduction of neuroinflammation.

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