Table 1.

The influence of pathogenic and nonpathogenic (phages) viruses on phagocyte functions.

Mechanism	Pathogenic Eukaryotic Viruses	Bacteriophages
Cytokine production	Epstein-Barr virus causes an increase in production of e.g., TNF-1α, IL-6, IL-8, IL-10 [73].	Lack of stimulation: IL-1α, IL-1β, IL-2, IL-6, IL- 10, IL-12, p40/p70, INT-γ, TNF-α (T4 phage and proteins on the surface of the phage head: gp23, gp24, Hoc, Soc) [45]. Inhibition of production of NFκB by human mononuclear cells induced by human herpesvirus-1 [74].
Chemotaxis of phagocytes	JEV stimulates production of the factor stimulating neutrophil chemotaxis by murine macrophages [75] influenza virus significantly decreased neutrophils migration activity [71].	Bacteriophage displaying neutrophil-binding peptide (FGP phage) stimulates neutrophil chemotaxis [76].
Phagocytosis of viral particles	Virions are phagocytosed by both neutrophils and monocytes e.g., Herpes virus is phagocytosed, and its envelope proteins are degraded [77]. Monocytes are faster at viral DNA degradation/digestion, neutrophils are more effective in phagocytosis.	Phage particles are phagocytosed by neutrophils, monocytes and dendritic cells [22,23,24,25,26,27].
Influence on phagocytosis	Active Mumps and the influenza viruses, inhibited the process of B. anthracis phagocytosis [78]. EBV reduced phagocytic activity of human monocytes, Influenza virus decreased phagocytosis of bacteria by human neutrophils [79,80] and murine macrophages [81] In HIV-positive patients the process of formation of the phagosome was impaired Coxsackie virus exerted an inhibitory effect on the ability of leukocytes to phagocytose, and it was dependent on the time of leukocytes’ exposure to the virus [82] Human neutrophils infected with HCMV increased expression of CD11 receptor (responsible for adhesion to the surface of vascular endothelial cells, migration, and phagocytosis of the particles opsonized with complement), resulting in increased phagocytosis [72]. Japanese encephalitis virus caused a reduction in phagocytosis of red dye by human neutrophils, there was no weakening of phagocytic activity for monocytes [83]. The Newcastle disease virus inhibited the phagocytosis of particles of red oil by: human neutrophils after stimulation with zymosan by and oxygen consumption after the stimulation of the cells with PMA, the activity of the membrane-bound enzyme NADPH was also decreased [84].	There was a weakening in phagocytosis of S. aureus by patients’ neutrophils which showed an initial decrease in the process [33].
Virions’ inactivation	Viral particles are absorbed into the interior of the phagosome, wherein the lysis takes place (e.g., inactivation of influenza virus by human neutrophils) [79].	It occurs in macrophages [22] and stimulated neutrophils (e.g., phage λ) [85].
Intracellular killing	Weakening in bactericidal activity of macrophages and neutrophil functions [80,81].	Lack of stimulation; lack of inhibition in vitro [35] and ex vivo [34].
Neutrophil degranulation	Respiratory syncytial virus causes neutrophil degranulation [86].	Neither the purified A3/R phage nor its lysate stimulates neutrophil degranulation [47].
Production of ROS	Sendai virus, influenza virus, cytomegalovirus, HIV caused the increased production of ROS by phagocytes (murine splenocytes, human neutrophils, monocytes) [69,70,71]. Sendai virus inactivated by ultraviolet light. Heat-inactivated virus did not stimulate the production of ROS. Only active viral particles stimulate the synthesis of ROS by phagocytes [70]. Weakened production by neutrophils and monocytes (HIV) [87].	Lowered production or lack of stimulation (e.g., T4, F-8, A3/R) [47].
Adsorption to phagocytes	Rotavirus, enter the host cells by using the interaction between the viral protein VP4 and αVβ3-integrin on the cell surface [88].	β-integrin [17].
Influence on apoptosis	Delay in apoptosis of human neutrophils infected with HCMV [83]. Acceleration of neutrophil apoptosis in HIV patients) [89].	No data.

TNF, Tumor necrosis factor; NFκB, Nuclear factor κB; JEV, Japanese encephalitis virus; EBV, Epstein-Barr Virus; HIV, Human Immunodeficiency virus; HCMV, Human Cytomegalovirus; PMA, Phorbol 12-myristate 13-acetate.