Enveloped viruses spread through both cell-free particles and direct cell-to-cell contacts. The latter mode accelerates viral dissemination and enables immune evasion by avoiding neutralisation of viral glycoproteins by human antibodies. Here, we compared the efficiency of these two transmission modes during SARS-CoV-2 infection. Target cells infected with a GFP-expressing reporter virus (cell-free infection) or cocultured with virus-producing donor cells (cell-to-cell transmission) showed similar proportions of GFP-positive cells and Remdesivir sensitivity. Both modes were equally affected by ACE2 neutralisation on target cells using monoclonal anti-ACE2 antibodies. However, inhibition of the serine protease TMPRSS2 by camostat strongly reduced cell-free infection but had limited impact on cocultures, suggesting a minor role for TMPRSS2 during cell-to-cell entry. Blocking endosomal entry pathways, including endosomal proteases or clathrin-mediated uptake, also restricted infection, yet substantially higher inhibitor concentrations were required to affect cell-to-cell transmission, indicating partial restriction of this route. We further assessed the sensitivity of both modes to humoral immunity. Monoclonal antibodies targeting the spike receptor-binding domain and sera from vaccinated or convalescent donors effectively neutralised cell-free infection in a concentration-dependent manner, whereas cell-to-cell transmission remained largely resistant to spike-directed neutralisation. Ongoing work uses electron microscopy to assess spike density at intercellular contacts and to determine whether this phenotype depends solely on spike expression or additional viral factors. Together, our data demonstrate that SARS-CoV-2 cell-to-cell transmission differs in cofactor usage and confers resistance to humoral immunity compared to cell-free infection.