Globalprevalence orincidence of coinfection among humans is unknown, but it is thought to be commonplace,[1] sometimes more common than single infection.[2] Coinfection withhelminths affects around 800 million people worldwide.[3]
Coinfection is of particular human health importance because pathogen species caninteract within the host. The net effect of coinfection on human health is thought to be negative.[4] Interactions can have eitherpositive or negative effects on other parasites. Under positive parasite interactions, diseasetransmission and progression are enhanced and this is also known assyndemism. Negative parasite interactions include microbial interference when one bacterial species suppresses thevirulence orcolonisation of other bacteria, such asPseudomonas aeruginosa suppressing pathogenicStaphylococcus aureuscolony formation.[5] The general patterns ofecological interactions between parasite species are unknown, even among common coinfections such as those betweensexually transmitted infections.[6] However,network analysis of afood web of coinfection in humans suggests that there is greater potential for interactions via shared food sources than via theimmune system.[7]
A globally common coinfection involvestuberculosis andHIV. In some countries, up to 80% of tuberculosis patients are also HIV-positive.[8] The potential fordynamics of these two infectious diseases to be linked has been known for decades.[9] Other common examples of coinfections areAIDS, which involves coinfection of end-stageHIV with opportunistic parasites[10] and polymicrobial infections likeLyme disease with other diseases.[11] Coinfections sometimes can epitomize azero sum game of bodily resources, and precise viral quantitation demonstrates children co-infected withrhinovirus andrespiratory syncytial virus,metapneumovirus orparainfluenza virus have lower nasal viral loads than those with rhinovirus alone.[12]
Poliovirus is apositive single-stranded RNA virus in the familyPicornaviridae. 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 viralgenomes within membrane vesicles, and transmission bybacteria 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 undergogenetic recombination when at least two viralgenomes are present in the same host cell. Kirkegaard and Baltimore[15] presented evidence thatRNA-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]
SomeCOVID-19 patients, or those who were ill with othercoronaviruses, can be co-infected with seasonalinfluenza (flu) viral strains, certain viral strains that cause thecommon cold, or can be co-infected withbronchitis orpneumonia from another bacterial or viral micro-organism. Even more dangerous, some of them could already have conditions liketuberculosis or activeAIDS 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.
^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.
^Di Perri, G; Cruciani, M; Danzi, MC; Luzzati, R; De Checchi, G; Malena, M; Pizzighella, S; Mazzi, R; et al. (1989). "Nosocomial epidemic of active tuberculosis among HIV-infected patients".Lancet.2 (8678–8679):1502–4.doi:10.1016/s0140-6736(89)92942-5.PMID2574778.S2CID5608415.