Global
prevalence or
incidence of coinfection among humans is unknown, but it is thought to be commonplace,[1] sometimes more common than single infection.[2] Coinfection with
helminths affects around 800 million people worldwide.[3]
Coinfection is of particular human health importance because pathogen species can
interact within the host. The net effect of coinfection on human health is thought to be negative.[4] Interactions can have either
positive or negative effects on other parasites. Under positive parasite interactions, disease
transmission and progression are enhanced and this is also known as
syndemism. Negative parasite interactions include microbial interference when one bacterial species suppresses the
virulence or
colonisation of other bacteria, such as Pseudomonas aeruginosa suppressing pathogenic Staphylococcus aureuscolony formation.[5] The general patterns of
ecological interactions between parasite species are unknown, even among common coinfections such as those between
sexually transmitted infections.[6] However,
network analysis of a
food web of coinfection in humans suggests that there is greater potential for interactions via shared food sources than via the
immune system.[7]
A globally common coinfection involves
tuberculosis and
HIV. In some countries, up to 80% of tuberculosis patients are also HIV-positive.[8] The potential for
dynamics of these two infectious diseases to be linked has been known for decades.[9] Other common examples of coinfections are
AIDS, which involves coinfection of end-stage
HIV with opportunistic parasites[10] and polymicrobial infections like
Lyme disease with other diseases.[11] Coinfections sometimes can epitomize a
zero sum game of bodily resources, and precise viral quantitation demonstrates children co-infected with
rhinovirus and
respiratory syncytial virus,
metapneumovirus or
parainfluenza virus have lower nasal viral loads than those with rhinovirus alone.[12]
Poliovirus
Poliovirus is a
positive single-stranded RNA virus in the family Picornaviridae. Coinfections appear to be common and several pathways have been identified for transmitting multiple virions to a single host cell.[13] These include transmission by virion aggregates, transmission of viral
genomes within membrane vesicles, and transmission by
bacteria bound by several viral particles.[citation needed]
Drake demonstrated that poliovirus is able to undergo multiplicity reactivation.[14] That is, when polioviruses were irradiated with UV light and allowed to undergo multiple infections of host cells, viable progeny could be formed even at UV doses that inactivated the virus in single infections. Poliovirus can undergo
genetic recombination when at least two viral
genomes are present in the same host cell. Kirkegaard and Baltimore[15] presented evidence that
RNA-dependent RNA polymerase (RdRP) catalyzes recombination by a copy choice mechanism in which the RdRP switches between
(+)ssRNA templates during negative strand synthesis. Recombination in RNA viruses appears to be an adaptive mechanism for transmitting an undamaged genome to virus progeny.[16][17]
Some
COVID-19 patients, or those who were ill with other
coronaviruses, can be co-infected with seasonal
influenza (flu) viral strains, certain viral strains that cause the
common cold, or can be co-infected with
bronchitis or
pneumonia from another bacterial or viral micro-organism. Even more dangerous, some of them could already have conditions like
tuberculosis or active
AIDS that make patients very vulnerable.
^Petney, TN; Andrews, RH (1998). "Multiparasite communities in animals and humans: frequency, structure and pathogenic significance". International Journal for Parasitology. 28 (3): 377–93.
doi:
10.1016/S0020-7519(97)00189-6.
PMID9559357.
^Crompton, DW (1999). "How much human helminthiasis is there in the world?". The Journal of Parasitology. 85 (3): 397–403.
doi:
10.2307/3285768.
JSTOR3285768.
PMID10386428.
^Shrestha, S. (2011). "Influence of host genetic and ecological factors in complex concomitant infections – relevance to sexually transmitted infections". Journal of Reproductive Immunology. 92 (1–2): 27–32.
doi:
10.1016/j.jri.2011.09.001.
PMID22019002.