Chemotherapy-induced peripheral neuropathy (CIPN) is the most prevalent neurological complication of cancer treatment which involves sensory and motor nerve dysfunction. Severe CIPN has been reported in around 5% of patients treated with single and up to 38% of patients treated with multiple chemotherapeutic agents. Present medications available for CIPN are the use of opioids, nonsteroidal anti-inflammatory agents, and tricyclic antidepressants, which are only marginally effective in treating neuropathic symptoms. In reality, symptom reappears after these drugs are discontinued. The pathogenesis of CIPN has not been sufficiently recognized and methods for the prevention and treatment of CIPN remain vulnerable to therapeutic problems. It has witnessed that the present medicines available for the disease offer only symptomatic relief for the short term and have severe adverse side effects. There is no standard treatment protocol for preventing, reducing, and treating CIPN. Therefore, there is a need to develop curative therapy that can be used to treat this complication. Melittin is the main pharmacological active constituent of honeybee venom and has therapeutic values including in chemotherapeutic-induced peripheral neuropathy. It has been shown that melittin and whole honey bee venom are effective in treating paclitaxel and oxaliplatin-induced peripheral neuropathy. The use of melittin against peripheral neuropathy caused by chemotherapy has been limited despite having strong therapeutic efficacy against the disease. Melittin mediated haemolysis is the key reason to restrict its use. In our study, it is found that α-Crystallin (an eye lens protein) is capable of inhibiting melittin-induced haemolysis which gives hope of using an appropriate combination of melittin and α-Crystallin in the treatment of CIPN. The review summarizes the efforts made by different research groups to address the concern with melittin in the treatment of chemotherapeutic-induced neuropathy. It also focuses on the possible approaches to overcome melittin-induced haemolysis. Graphic Abstract

Coronavirus disease 2019 (COVID-19) is a potential health threat in the highly mobile society of the world. Also, there are concerns regarding the co-infections occurring in COVID-19 patients. Herpes zoster (HZ) is now being reported as a co-infection in COVID-19 patients. It is a varicella-zoster virus induced viral infection affecting older people and immunocompromised individuals. Reactivation of HZ infection in COVID-19 patients are emerging and the mechanism of reactivation is still unknown. A most convincing argument would be, increased psychological and immunological stress leading to HZ in COVID-19 patients, and this review justifies this argument.

The life cycle of Herpes simplex virus starts with attachment to the host cell, injection of nucleocapsid into the cytoplasm, replication, transcription and viral protein production, and finally the assembly of the mature virion nucleopcapsid. The assembled nucleocapsid exits the host nucleus and gains a tegument layer bound within a bilayer of membrane phospholipid. The packaged virion particle then exits the host cell. The interaction of the (Deoxyribonucleic acid) DNA packaging complex- terminase, present on the mature viral nucleocapsid, with other proteins involved in nuclear egress and cytoplasmic tegumentation has led to the proposal of the model by which the terminase complex may be involved in these two events. The role of terminase complex in Herpes Simplex Virus (HSV) genomic DNA encapsidation into the capsid is previously established, but the role of the terminase subunits post DNA packaging remains unclear. The current review provides a model by which the terminase complex may have a role to play in the events of nuclear egress and secondary envelopment.