Transmission of simian immunodeficiency virus (SIV) of the chimpanzee to humans has occurred at least four times leading to HIV-1 groups M, N, O, and P. Notably, in contrast to other retroviruses, the risk of transmission of SIV by bite appears to be very low [19]. Whether SIV transmission to humans resulted from bite or other modes of transmission remains unclear.
Definite proof of HIV transmission by human bite remains difficult as reliable exclusion of other risk factors depends on truthful statements of the patients. Minimum information includes severity of the lesion, documented seroconversion of the bite victim shortly after the incident, as well as the HIV-viral load of the aggressor on the date of the bite. Nucleic acid sequencing of the viruses from the aggressor and bite victim should indicate close relatedness. However, limitations of comparative analysis of nucleic acid sequencing have to be considered, in particular after longer time periods between incident and examination.
In our opinion, at least five cases support the hypothesis that human bites may have caused HIV-1 transmission (cases 4, 6, 9, 10, and 11). In these cases, comparison of viruses from aggressors and victims showed closely related nucleic acid sequences, suggesting a common ancestor virus.
A deep bleeding wound of the victim appears to be the primary risk factor. A high viral load and bleeding oral lesions are mostly present in the aggressor (Table 1). With the exception of one case, available HIV-1 viral loads were at least 17,163 copies/ml plasma. In some reports, information on the viral load was missing, but the aggressor suffered from AIDS without receiving ART, suggesting a high viral load.
Recently, HIV-1 transmission by bite was reported from an HIV-infected person who had started HAART 6 weeks prior to the bite and had a viral load of 200 copies/ml (2.3 log10) 29 days thereafter (case 10). Fourteen months prior to the incident, his viral load had been 15,849 copies/ml (4.2 log10). This suggests that HIV-1 may also be transmitted with low viral loads if there are deep bite wounds.
Poor oral hygiene or bleeding gums associated with free blood in saliva, with HIV-containing lymphocytes and cell-free HIV, evidently increase the risk of HIV transmission by bite and have even been considered to be a precondition for transmission. Whether HIV transmission may also occur via saliva only remains speculative, but appears to be possible. In one case HIV-1 transmission appears to have occurred via saliva without contamination of blood (case 9).
Viral load in saliva parallels that in plasma, but is usually 1–2 log lower than in matched plasma samples. However, high plasma viral loads may be associated with saliva viral loads from 2.6 up to 5.9 log10 copies/ml [20]. Periodontal disease and gingival inflammation can even lead to salivary viral hyper-excretion with a fourfold or higher viral load in saliva than in plasma in individual cases [21]. Oral cavity may become an HIV-1 reservoir in individual cases.
The primary reason for the low HIV transmission risk by human bite appears to be that saliva is normally hypotonic. Hypotonicity was proven to rapidly kill infected mononuclear leukocytes, the main source of infectious HIV in the mouth. It also prevents their attachment to mucosal epithelial cells and replication of infectious HIV-1, thereby preventing transmission [22]. Cell-free HIV-1 in the mouth is inactivated by salivary inhibitors and neutralizing antibodies and usually non-infectious. However, the risk of transmission increases when saliva becomes isotonic by shed blood and when the viral load of cell-free HIV-1 in blood is high. Isotonic saliva was shown to improve the survival of infected mononuclear leucocytes, increase virus replication in the mouth, and promote cell-to-cell transmission [22].
We believe that the risk of HIV transmission by human bite should be addressed in PEP guidelines, even if the risk appears to be overall very low [2]. The number of reported cases is small, but there may have been some underreporting, particularly in high-prevalence populations of HIV infection. PEP should be recommended when a bite has led to an open skin lesion manifesting as a bleeding wound, and when the aggressor is known to be HIV-positive [2, 18]. PEP has been missed in this presented case as well as in two previously reported bite victims (cases 9 and 10). Transmission of HIV has still a lifelong impact on our patients’ lives, while PEP has become tolerable, cost-effective, and safe nowadays [23].