The pandemic caused by severe acute respiratory syndrome coronavirus 2 is sweeping the world, threatening millions of lives and drastically altering our ways of living. According to current studies, failure to either activate or eliminate inflammatory responses timely and properly at certain stages could result in the progression of the disease. In other words, robust immune responses to coronavirus disease 2019 (COVID-19) are critical. However, they do not theoretically present in some special groups of people, including the young, the aged, patients with autoimmunity or cancer. Differences also do occur between men and women. Our immune system evolves to ensure delicate coordination at different stages of life. The innate immune cells mainly consisted of myeloid lineage cells, including neutrophils, basophils, eosinophils, dendritic cells and mast cells; they possess phagocytic capacity to different degrees at different stages of life. They are firstly recruited upon infection and may activate the adaptive immunity when needed. The adaptive immune cells, on the other way, are comprised mainly of lymphoid lineages. As one grows up, the adaptive immunity matures and expands its memory repertoire, accompanied by an adjustment in quantity and quality. In this review, we would summarise and analyse the immunological characteristics of these groups from the perspective of the immune system ‘evolution’ as well as ‘revolution’ that has been studied and speculated so far, which would aid the comprehensive understanding of COVID-19 and personalised-treatment strategy.

Immunosuppressive viral diseases have become a major cause of mortality and economic losses in poultry industry mainly because of increased susceptibility of second bacterial infections and low response to vaccination. Nowadays chicken infectious anaemia is a great threat to poultry industry due to the large number of deaths and immuno-suppression it causes. Chicken anaemia virus replicates in erythroid and lymphoid progenitor cells, causing an apparent, sub-clinical infection that leads to depletion of these cells with consequent immunosuppressive effects. This review will summarise the currently available information about the chicken infectious anaemia virus and subsequent disease. Secondly, it will address the possible immune-pathogenic and immune-suppressive effects of chicken infectious anaemia in birds, including commercial poultry. Finally, the future prospects of vaccination against chicken infectious anaemia and other possible novel methods for the control of chicken anaemia virus are discussed.

Malaria kills approximately 1–2 million people every year, mostly in sub-Saharan Africa and in Asia. These deaths are at the most severe end of a scale of pathologies affecting approximately 500 million people per year. Much of the pathogenesis of malaria is caused by inappropriate or excessive immune responses mounted by the body to eliminate malaria parasites. In this review, we examine the evidence that immunopathology is responsible for malaria disease in the context of what we have learnt from animal models of malaria. In particular, we look in detail at the processes involved in endothelial cell damage leading to syndromes such as cerebral malaria, as well as generalised systemic manifestations such as anaemia, cachexia and problems with thermoregulation of the body. We also consider malaria in light of the variation of the severity of disease observed among people, and discuss the contribution from animal models to our understanding of this variation. Finally, we discuss some of the implications of immunopathology, and of host and parasite genetic variation, for the design and implementation of anti-malarial vaccines.