Dr. Barbara Tonini (*) DVM, freelance, Milan
FIV infection may remain subclinical for long periods, so without causing any symptoms, but leads to the development of clinical manifestations such as, generalized lymphadenopathy, diarrhea, anorexia, fever, weight loss, chronic infections, neurological disorders and cancers.
FELINE IMMUNODEFICIENCY VIRUS (FIV)
The feline immunodeficiency virus (FIV) is a disease caused by a lentivirus, subfamily of retroviruses, which in cats leads to acquired immunodeficiency syndrome (Pedersen et al, 1987).
Although FIV infection can remain sub-clinical for long periods, thus without causing any symptoms, it leads to the development of clinical manifestations such as, generalized lymphadenopathy, diarrhea, anorexia, fever, weight loss, chronic infections, neurological disorders and cancers ( Fleming et al, 1991; Shelton et al, 1995).
Despite the lack of clinical signs during the asymptomatic period there has been a progressive decline in immune function. This decline is attributable to a generalized cytopenia, which mainly is expressed with a depletion of CD4 + lymphocytes and a reduction in the ratio of CD4 + / CD8 + (Callanan et al, 1992), that an alteration of neutrophil function (Kubes et al , 2003).
The infection immunosuppression resulting from IVF involves therefore a greater susceptibility to opportunistic pathogens that cause chronic disease processes often resistant to antimicrobial therapy. Therefore, the therapy of IVF is a support therapy to limit the secondary complications that often result from opportunistic infections.
FIV AND IMMUNE DYSFUNCTION
Feline immunodeficiency virus (FIV) causes a progressive decline of the immune response that leads to a Acquired Immunodeficiency Syndrome comparable human immunodeficiency (HIV).
FIV infection causes an initial immune response to reduce plasma viremia but that often does not permanently remove the virus that causes inadequate cell-mediated immune response, evident especially to secondary pathogens.
Secondary pathogens, according to recent studies, can lead to the development of disease conditions before it is evident the decrease in the number of CD4 + lymphocytes (Tompkins, 2008).
So how can we slow down the progression of disability and reduce the onset of secondary infections?
The answer is simpler than expected because the goal is to optimize the health of our patients, especially if at increased risk of disease.
In this regard, a prominent place in the immunodeficiency complications management is occupied by appropriate nutrition management, preventing and treating malnutrition.
In fact, the decreased intake of food, which can also occur in asymptomatic subjects, however, is very frequent during the symptomatic phase of the disease, due to both inadequate food intake (anorexia, nausea, oral disease), that the malabsorption and the hyper catabolism secondary to the infection itself and / or to opportunistic infections.
For a good immunostimulatory effect we have to think not only to a correct administration of macronutrients, but also of micronutrients (minerals and vitamins) that provide strategic body of the profits of defense instruments.
Among the micronutrients with “therapeutic” effect an important role is exerted by the zinc which, intervening in numerous enzymatic reactions, allows the body to more effectively combat the virus assault and bacteria
ZINC AND IMMUNE DEFICIENCY
Zinc is a trace element that plays a central role in the immune response and is in fact known as subjects with zinc deficiency have an increased susceptibility to various pathogens.
The immunological mechanisms by which zinc influences the immune response are many and range from the integrity of the skin barrier to gene regulation of T lymphocytes
Zinc plays a crucial role in the normal development and function of cells that regulate the non-specific immunity: neutrophils and natural killer (Ibs and Rink, 2003). In addition, zinc deficiency affects the development and the acquired immunity activity, preventing either the production of T lymphocytes that some important functions, such as the activation and cytokine production. Similarly, the deficiency impairs the development of B lymphocytes and the production of antibodies. Finally, macrophages, essential for numerous immunological functions, have impaired phagocytosis and the production of cytokines (Shankar, Prasad, 1998).
The T cells are undoubtedly the most sensitive immune cells to zinc depletion and ongoing shortages compromised their multiplication and subsequent differentiation into Th1 lymphocytes (Fraker and King, 2004; Overbeck et al, 2008) (Figure 1).
For these reasons, it is known that zinc deficiency, negatively influencing the immune response may increase the frequency of opportunistic infections, infections caused by low virulent or pathogenic microorganisms normally maintained in a state of latency.
Therefore in a subject immunocompromised, in whom there is already an increased vulnerability to secondary infections, can be deduced how immune consequences of zinc deficiency are more serious.
ZINC: PROTECTIVE AND THERAPEUTIC ROLE
From the experience of human medicine it is understood that zinc supplementation in subjects suffering from HIV reduces the frequency of secondary infections and that, as a result of the normalization of plasma zinc levels, there is a slowing of the progression of the disease. In particular, the feeding of children in developing countries living with HIV has resulted in the reduction in the number and duration of episodes of pneumonia and diarrhea (Bhutta et al, 1999; Bobat et al, 2005).
Given the high degree of similarity between the HIV human immunodeficiency virus and feline immunodeficiency virus FIV, the results obtained by the administration of zinc with HIV could also be observed in cats with FIV.
The administration of zinc, allowing better management of secondary infections that are often refractory to antibiotic therapy, might be an important therapeutic aid in cats infected by FIV. Therefore the integration utility of zinc on the immune response in infectious diseases can be derived not only for the multitude of biological functions in which it is involved, but also for the widespread prevalence of conditions in which occurs a subclinical deficiency of this mineral.
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