Zinc and Infectious Diseases

Numerous animal studies indicate that Zn deficiency decreases resistance to a range of bacterial, viral, fungal and parasitic pathogens (for a review, see Shankar and Prasad, 1998), probably because of the immune impairments induced by the deficiency. Thus, the enhancing effect upon the immune response of providing Zn should translate into improved host defence and increased resistance to pathogens. However, most microorganisms require Zn for basic cellular processes (e.g. replication) and, during the acute-phase response, Zn is redistributed from the plasma to the liver and to lymphocytes (see Shankar and Prasad, 1998). It has been suggested that this is an adaptive response intended to deprive invading pathogens of Zn, facilitate immune function and prevent free-radical damage to cells. However, plasma Zn levels resulting from the acute-phase response remain generally well above the levels at which the growth of most pathogens is affected. The balance between Zn availability for host immunity and for the invading pathogen is affected by multiple factors. It appears, however, that in most cases any benefit to the pathogen of Zn availability is well compensated by the concomitant improvement in host immune function.

A number of studies have demonstrated the benefits of Zn supplementation in regard to infectious diseases in human populations (for a review, see Shankar and Prasad, 1998). Controlled trials of Zn supplementation demonstrated a reduction in the incidence and duration of acute and chronic diarrhoea by 25-30%, and in the incidence of pneumonia by up to 50% (Castillo-Duran et al., 1987; Sazawal et al., 1995, 1996, 1998; Ninh et al., 1996; Rosado et al., 1997; Roy et al., 1997, 1999; Ruel et al., 1997). Some studies implied that Zn may reduce clinical disease caused by Plasmodium falciparum (Gibson et al., 1991; Bates et al., 1993), and it has been demonstrated in a controlled trial carried out in Papua New Guinea that Zn supplements could reduce health-centre attendance attributable to malaria by over 35% (Shankar et al., 1998). Decreased Schistosoma mansoni egg counts were observed among children given Zn supplements versus those given a placebo (Friis et al., 1997). Humans suffering from AE also suffer fewer infections when given supranormal levels of Zn, and plasma Zn levels are substantially lower in patients with diffuse leproma-tous leprosy compared with those with the more limited bacillary form (for references, see Shankar and Prasad, 1998). Zn deficiency is frequently seen in patients with human immunodeficiency virus (HIV), and disease progression is accompanied by decreased serum Zn levels and depressed lymphocyte mito-genic responses (Pifer et al., 1987; Falutz et al., 1988; Wang et al., 1994). These changes are partially reversible by Zn supplementation.

The role of Zn in preventing and treating the common cold has been discussed for many years. It appears that Zn is effective in reducing the severity of cold symptoms. For example, in a recent placebo-controlled study, 12.8 mg of Zn was administered in lozenges to a group of subjects every 2 to 3 h while awake within 24 h of developing symptoms of the common cold (Prasad et al., 2000). In the Zn-treated group, the duration and severity of cold symptoms were decreased approximately 50% in comparison with the placebo group.

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